Wound Healing Flashcards
Chemotactic Agents
Substances that attract cells necessary for wound repair after an injury.
Chemotaxis
The process of active movement toward the area of highest concentration of a chemical signal.
Angioblast
Endothelial cell that lines the vessel wall
Basophil
Granular leukocyte which releases chemicals such as histamine which are responsible for inflammation and heparin.
Collagenase
Endogenous enzyme that breaks down collagen during the maturation and remodeling process of wound healing.
Contraction
Part of the proliferative phase of wound healing decreasing the size of the wound defect. Myofibroblasts drive the process of wound contraction.
Cytokine
Signaling protein with role in the inflammatory phase of wound healing..
Regulates cell proliferation, migration, matrix synthesis, deposition, degradation.
All are cytokines: interferon, growth factors, interleukins, tumor necrosis factor, platelet derived growth factor.
Diapedesis
The movement of PMN through capillary walls by extending foot like projections through the narrow openings within the vessel walls.
Epithelialization
Resurfacing of the wound with keratinocytes.
Exudate
Fluid containing high levels of protein and cells.
Fibroblasts
Dermal cells that produce collagen, elastin, granulation tissue and growth factors. Responsible for forming granulation tissue
Granulation tissue
Temporary structure composed of vascularized connective tissue that fills the wound void.
Growth Factor
Growth promoting substance that increases or enhances cell size, proliferation or activity.
Histamine
Chemical mediator released by mast cells which cause vasodilation, increase vessel wall permeability, and attracts other cells to the area.
Hyaluronic acid
Key structural and functional component of the extra cellular matrix which promotes cell proliferation, and tissue regeneration and repair. Hyaluronic acid is a key component of amniotic fluid.
Inflammation
First phase of wound healing, characterized by rubor, calor, tumor, dolor, and functio laesa; vascular and cellular response to healing.
Integrin
Cell surface receptor that allows cells to reversibly bind to the extra cellular matrix.
Margination
Process in which PMNs are pushed to the sides of a vessel wall.
Mast cell
Cell that helps to initiate inflammation, secretes histamine, enzymes, and destroys bacteria and debris.
Matrix Metalloprotease (MMPs)
Protease that degrades the extra cellular matrix formed during the inflammatory process.
Secreted from: keratinocytes, neutrophils, macrophages, fibroblasts.
Maturation and remodeling
The third phase of wound healing during which collagen matures and reorientation along the lines of stress.
Myofibroblast
Cell possessing properties of fibroblasts and smooth muscle cells which cause wound contraction.
Polymorphonuclear Neutrophil (PMN)
Cell that cleans the wound; secretes enzymes. MMPs and inflammatory mediators.
First cells to the site of injury. Scavenger. Kills bacteria.
Platelet
Cell that controls bleeding but also releases growth factors and chemotactic agents.
Proliferation
Second phase of wound healing; building and regenerating phase consisting of angiogenesis, granulation tissue formation, wound contraction and epithelialization.
Prostaglandin
Substance released from injured cells causing vasodilation
Regeneration
Re-epithelialization of a wound; principal method of healing in primary intention.
Remodeling Repair
The final phase of wound healing in which scar tissue is reorganized. Primary mode of wound closer by secondary intention.
Scab
Collection of necrotic cells, fibrin, collagen, and platelets that covers a superficial wound.
Thrombocyte
Also known as a platelet
Tissue inhibitors of matrix metalloproteas (TIMPs)
Protease inhibitor of MMPs
Transudate
Low protein collection of fluid caused by increased permeability
Wound contracture
Process by which myofibroblasts pull wound margins closer together thereby decreasing the size of the defect.
Macrophage
- Directs repair process.
- with killing bacteria and cleaning wound.
- Secretes growth factors and MMPs
TIME principles in wound bed preparation
T- tissue nonviable or deficient. This defective matrix and cell debris impairs healing.
Clinical action- debridement
Time Principles of wound bed preparation.
I- infection or Inflammation. High bacteria counts or prolonged inflammation secondary to :
- inflammatory cytokines
- increase proteases
- decreased growth factor activity
Action- antimicrobials, antiinflammatories, protease inhibitors.
TIME Principles of wound bed preparation.
M- moisture balance. Desiccation slows epithelial migration. Excessive fluid causes maceration.
Action- moisture balance dressing, compression, negative pressure dressing,
TIME principles of wound bed preparation.
E- edge margin non-advancing or undermined. Epidermal margin non-advancing or undermined.
Use Adjunctive therapies, bioengineered skin, debridement, skin grafts.
DIME
D-debridement
I-infection/inflammation
M-moisture
E- wound edge margin
Bioburdon
Number, diversity and virulence of bacteria present in a wound, as well as the interaction of organisms with each other. Excessive bio burden inhibits wound healing.
Cheryl at early alcohol
Emulsifier present in some creams and paste bandages which may cause an allergic dermatitis.
Acute wound
Caused by surgery or trauma in a healthy individual. Less than 2 weeks old.
Chronic Wound
Wound induced by various causes, whose progression through the phases of wound healing is prolonged or arrested die to underlying conditions.
Granulocytes
BEN
Basophils
Eosinophils
Neutrophils
Eosinophils
Immune regulators. Fight infection by destroying parasites and bacteria. Along with mast cells they control allergic responses
Agranulocytes
Monocytes, when they leave the circulation, they become macrophages.
Lymphocytes
B cells- make antibodies
T cells fight viruses
NK (natural killer cells) fight viruses
Agranulocytes
Monocytes, when they leave the circulation, they become macrophages.
Lymphocytes
B cells- make antibodies
T cells fight viruses
NK (natural killer cells) fight viruses
