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wound healing

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Important enzymes involved in cleaving paths throughout the mesh are
matrix metalloproteinases (MMP's), modulated by their inhibitors
Transforming growth factor (TGF)
which stimulates keratinocytes.
TGF-b may be the most
potent stimulant of collagen synthesis
Fibrin is broken down as part of this clean-up and the degradation products attract the next cell type involved
macrophages
Cell surface receptors of the integrin superfamily
help cells respond to chemical signalsthat are generated by a wound.
New vessel formation is stimulated by
high lactate, acid pH, and low tissue oxygen in wounds.
Stem cells provide
the migration of cells from the periphery of the wound and adnexal structures.
The macrophages orchestrate the multiplication of endothelial cells with
the sprouting of new blood vessels, the duplication of smooth muscle cells, and the creation of the milieu secreted by the fibroblast. (FGF, EGF, PDGF)
neutrophils
are the first leukpcytes to migrate during inflammation and provide earliest proinflammatory cytokines
proliferative phase manifest as
pebbled red tissue
vascular endothelial growth factor,VGEF, is
the most potent angiogenic agent identified besides cytokines
Numerous enzymes and cytokines are secreted by the macrophage
Collagenases, Interleukins (IL) and tumor necrosis factor (TNF), Transforming growth factor (TGF)
Interleukins (IL) and tumor necrosis factor (TNF)
stimulate fibroblasts (produce collagen) and promote angiogenesis
Macrophages also phagocytize bacteria and release a variety of chemotactic
direct the proliferative phase of wound healing
capillary leak
after vasoconstriction; along with vasodilation allows serum and leukocytes into field of injury, secondary to histamine release, cells of inflammation migrate to wound bed
PMNs are responsible for
scavenging (phagocytizing) bacteria and debris, complement-mediated opsonization of bacteria and destruction of bacteria via oxidative burst mechanisms (superoxide and hydrogen peroxide formation)
contribute to vessel permeabilty
histamine, prostaglandins, kinins, C3a, C5a, luekotrienes
Collagenases released by macrophages during inflammation
debride the wound
Angiogenesis is the product of parent vessel offshoots. The formation of new vasculature requires
extracellular matrix and basement membrane degradation followed by migration, mitosis, and maturation of endothelial cells.
thrombin
inc vascular permeability and helps migration of inflammatory cells
In days 5-7
fibroblasts have migrated into the wound, laying down new collagen.
the most important mesenchymal cell involved in wound healing
fibroblasts
Other chemotactic agents are released during inflammation
fibroblastic growth factor (FGF), transforming growth factors (TGF-β and TGF-α), PDGF, and plasma-activated complements C3a and C5a (anaphylactic toxins)
Cell migration is facilitated by
hyaluronic acid in the wound.
hemostasis/inflammatory phase
vasoconstriction, hemostasis, capillary leak, inflammation

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