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Phys. of healing
WOCN program
Question | Answer |
---|---|
List factors that affect wound healing | Layers involved (full vs partial) onset and duration (acute vs chronic) and type of wound closure (1* vs 2*)age, co-morbidity, obesity, smoking |
Differentiate between partial and full thickness wounds | Partial effects the epidermis and superficial dermis, full thickness extends through the dermis and beyond |
Describe healing by primary intention | Edges are well approximated, low bacterial load, minimal connective tissue repair needed, skin returned to full function, heals quickly |
What are the roles of growth factors in wound healing | regulate division, proliferation and differentiation of non immune response cells |
What are the roles of cytokines in wound healing | direct the function of cells of the immune response, inflammation, and hematopoesis- |
What are the roles of proteases in wound healing | Destruction of damaged proteins, destr. Of provisional ECM, |
What are the wound healing phases | Hemostasis, inflammatory, proliferative, maturation/remodeling |
Identify 2 mechanisms of wound healing | Regeneration or scar formation |
Describe the tissues layers involved in partial thickness wound | Epidermis and superficial dermis |
Describe the key mediators involved in partial thickness wound | Epithelial cells |
Describe the critical events in the repair process involved in partial thickness wound | inflammation, epithelial resurfacing, restoration of epithelial thickness and skin function |
What is the approximate time frame for each wound healing phase with a full thickness wound? | hemostasis-0-1 hr inflammation:1-3 days proliferative: epithelialization hours to 2 days, granulation day 3 to 21 days maturation 21 days remodeling-months |
What is neoangiogenesis | req's stim by GF's, production of new vessels by growth and differentiation of local endoth. cells, recruitment of stem cells to to form new vessels de novo |
Explain the process of collagen synthesis | coll. molecule undergoes a series of intracellular changes, is secreted into ECM as procollagen, cross linking is the critical part for tensile strength |
Describe the differences between acute and chronic wounds | CAUSE (sudden, traumatic vs slow onset, disease, repetitive injury)TIME (rapid and predictably vs prolonged) CLOSURE (durable vs non-durable) |
What are 7 systemic factors that effect wound healing | perfusion/oxygenation, smoking/tobacco use, nutritional status, DM, obesity, medications, advanced age, immunosuppression, stress |
Define the difference between growth factors and cytokines | GF's regulate non immune cells to proliferate, differentiate. cytokines regulate interaction between immune cells (immunity, inflammation, hematopoesis) |
Explain islets in partial thickness repair | Exposed basement membrane that is a source of new epithelium |
Why is partial wound painful | Nerves are exposed |
List the major components of partial thickness repair | Inflammation, Epithelial resurfacing, restoration of epithelial thickness and function |
What is the term used to describe the process when migrating epidermal cells contact one another? | contact inhibition |
After epidermal cells contact other epidermal cells, the next process is: | upward migration begins |
First response to tissue injury is: | Hemostasis |
How long does the first response to tissue injury last if there are no complications? | 24 hrs or less |
What is the difference in a wound that dries out as compared to a wound that stays moist? | moisture facilitates migration of cells, dried requires lysis of bonds to scab to provide moist pathway under scab (delays healing) |
Full thickness wounds can be either acute or chronic: true or false | True |
A hallmark outcome of the proliferative phase is the formation of: | Formation of Granulation tissue |
Identify one medical condition that can prolong the inflammatory phase | Diabetes |
List the four phases of healing for a full thickness wound by secondary intention | No hemostasis, inflammation, proliferation and remodeling |
What happens during the hemostasis phase | Clots of fibrin, blood cells and platelets form and block the blood flow, histamine released cytokines and growth factors released, brief vasoconstriction, coag intrinsic and extrinsic pathways triggered, chemoattraction of neutrophils & macrophages |
What happens during the inflammatory phase in primary intention | Cleans the wound bed- margination and diapedesis, phagocytes remove bacteria and debris, macrophages continue phagocytosis and release growth factors, stimulate angiogenesis, fibroblast migration, tissue synthesis lasts 3 days usually |
What happens during the proliferative phase with primary intention | Epithelialization, granular tissue formation, neoangiogenesis, matrix deposition and collagen synthesis, wound contraction, |
What happens during the maturation/remodeling phase | fibroblasts synthesize conn. tiss. proteins for provisional ECM, # of binding sites for fibroblasts increases, (upregulation by PDGF) can last a year |
The tensile strength of remodeled ECM is never more than __% of the tensile strength in non wounded tissue | 80% of nonwounded tissue |
A closed non-proliferative wound edge is known as a ____ | Epibole |
List three characteristics of a chronic wound | Prolonged inflam phase, deficiency of GF receptor sites, cellular senescence, high levels of proteases, high levels of MMP's, stalled healing, biofilm |
Define the difference between keloid scars and hypertrophic scars | Hypertrophic- at site of wound, collagen well organized, myelofibroblasts present, can regress in time. Keloid- collagen disorganized, not limited to wound site, high # receptors growth factors, no myelofibroblasts no balance of synth./degradation |
Distinguish the difference between cytokines and growth factor | Growth factors regulate growth, proliferation and differentiation of cells, cytokines regulate the functions Cytokines work with immune cells, GF's work on non immune cells regulate function and wound repair |
The FDA approved PDGF for treatment of ______ ulcers | diabetic foot ulcers |
Explain the difference in molecular environment of chronic wounds and healing wounds | Chronic: high level of proteases, inflamm. Cytokines, bacterial load (biofilm) low mitogenic activity, senescent cells. Acute: high mitogenic activity, low inflamm cytokines, low proteases, intact functional ECM, cells active not quiet. |
Explains the principle of wound bed preparation by the TIME method | Tissue (nonviable or deficient), Infection or inflammation, Moisture balance, Edge of wound (advancing or undermining) |
Give an example of a topical dressing that can chemically bind to members of the MMP family that will reduce protease levels in chronic wounds | promogran |
Characteristics of a chronic wound | Prolonged inflammatory and proliferative phases, failure to close in a timely manner or failure to produce a durable closure, caused by compromise of come sort (vascular, repetitive injury, infection) |
Secondary intention | Wound left open and allowed to heal by scar formation |
Tertiary intention | Wound closed after a period of being left open aka (delayed primary closure) |
List the stages of healing a full thickness wound by primary intention | Hemostasis, inflammation, proliferation (limited need 2* primary closure) maturation/remodeling |
What affects duration and intensity of inflammatory stage | Bacterial load, amt. of devitalized tissue, diabetes, some ECM components |
MMP's | Matrix metalloproteases- degrade provisional ECM can be pro-inflammatory or anti-inflammatory |
A wound that is left open to heal by repair or scar formation is classified as healing by ___ | secondary intention |
What role does moisture play in a partial thickness wound | moist pathway required for cell migration, scab requires cleaving of bonds to create moist pathway, this delays healing |
Describe the tissues layers involved in full thickness wound | epidermal, dermal, possibly hypodermis and below |
Describe the repair process of a full thickness wound healing by primary intent | homeostasis, inflammation, proliferation (epithelialization, granulation) maturation/remodeling neoangio. & connective tiss. synthesis simultaneous and codependent |
Describe the key mediators in a full thickness wound | bioactive molecules-(cytokines, GF's) Matrix proteins,(MMP's, TIMP's, ADAMs) ECM, host factors |
Describe the critical events in the repair process of a full thickness wound | hemostasis (if acute) inflammation, proliferation (epithilalization, granulations) maturation/remodeling |
What is the approximate time frame for each wound healing phase with acute full thickness wound | hemostasis: 0--Inflammation:0-7 days proliferation 7-17 days: maturation/remodeling: 17-25 |
Describe the wound healing phases | hemostasis-stops bleeding, initiates repair cascade, stimulates intrinsic and extrinsic anti coag. Inflamm.cleans wound bed, (neutrophils/macrophages) Proliferation (granulation tissue syntheses) remodeling/maturation-alignment of collagen |
Describe healing by secondary intention | wound is left open, allowed to heal by scar formation, more prone to infection, heals slo wly, inflamm. and prolif. phases prolonged |
What is the difference between healing by primary intention and secondary intention | 1* intention:edges approximated(sutures or staples), restores skin to FUNCTION, 2* wound left open heals by scar formation |
VEGF | vascular endothelial growth factors promotes angiogenesis |
what affects neoangiogenesis | oxygenation, hyperglycemia, CAD, chemo, RT, aging, diabetes, female sex |
how does tobacco use effect repair | decreases oxygenation, increases platelet aggregation, impairs immune response, reduced fibroblast activity, higher infection rates |
how does oxygenation effect repair | initial hypoxia stimulates fibroblast proliferation and angiogenesis |
TIMPs | TIMP tissue inhibitor of metalloproteinases reduces cytokine release by decreasing ADAMs |
ADAMs | a disintegrin and metaloproteinase- promotes the release of a particular cytokine |
what are interventions to improve wound perfusion | hydration, warmth, oxygenation, no smoking, pain and stress control, eliminate edema |
what cells are the key mediators in partial thickness wound repair | epithelial cells |
PDGF | platelet derived growth factors |