WOUND HEALING Flashcards
(43 cards)
Precedes and initiates inflammation with the ensuing release of chemotactic factors from the wound site.
Hemostasis
The first infiltrating cells to enter the wound site, peaking at 24-48 hours. Primary role of this is phagocytodis of bacteria and tissue. debris
PMN
The 2nd population of inflammatory cells that invades the wound. Achieve significant numbers in the wound by 48-96hrs post injury and remain present until wound healing is complete. Central function is activation and recruitment of other cells via mediators such as cytokines and growth factors.
Macrophages
Peak at 1 week post injury and truly bridge the transition from the inflammatory to the proliferative phase of healing. Plays an active role in the modulation of the wound environment.
Lymphocytes
Next phase to hemostasis and inflammation which spans 4 through 12 days. Fibroblasts and endothelial cells are the last cell populations to infiltrate the healing wound.
Proliferates
TThe strongest chemotactic factor for fibroblasts is
PDGF
Proliferate extensively or participate in angiogenesis)
Endothelial cells
The most abundant protein in the body
Collagen
The major component of extracellular matrix of the skin
Type I collagen
Type of collagen becomes more important during the repair process
TYpe III
Comprise a large portion of the “ground substance” that makes up granulation tissue. The major types present in wounds are dermatan and chondroitin sulfate
Glycosaminoglycans
Begins during the fibroplastic phasae and is characterized by a reorganization of previously synthesized collagen
Maturation and Remodeling
Pattern of desposition of matrix:
- Fobronectin and collagen type III constitute the early matrix scaffolding
- Glycosaminoglycans represent the next significant matrix components
- Collagen type I is the final matrix
The final step in establishing tissue integrity. It is characterized primarily by proliferation and migration of epithelial cells adjacent to the wound.
Epithelization
All wounds undergo some degree of this. For wounds that do not have surgically appx. edged, the area of the wound will be decreased by this action.
Wound Contraction
Postulated as the major cell responsible for contraction. It differs from the normal fibroblast in that it possesses a cytoskeletal structure
Myofibroblast
Types of Ehlers - Danlos Syndrome:
Skin: thin, translucent, visiblr veins, normal scarring, no hyperentennsibility; no joint hypermobility; arterial, bowel and uterin rupture. Type III collagen defect.
Type IV
Types of Ehlers - Danlos Syndrome:
Skin: sofy, hyperextensible, easily bruising, fragile, atrophic scars; hypermobile joints; varicose veins; premature births
Type I
Types of Ehlers - Danlos Syndrome:
Similar to Type II but inheritance is XLR
Type V
Types of Ehlers - Danlos Syndrome:
Similar to Type I, but less severe
Type II
Types of Ehlers - Danlos Syndrome:
SKin: soft, not hyperextensible, normal scars; small and large joint hypermobility
Type III
Types of Ehlers - Danlos Syndrome:
Hypermobile joints, skin fragility. Absence of tenasein X protein.
TNx
Types of Ehlers - Danlos Syndrome:
Similar to Type II with abnormal clotting studies. Fibronectin defect.
Type X
Types of Ehlers - Danlos Syndrome:
Skin: soft, ;ax; bladder diverticula and rupture; limited pronation and supination; broad clavicle; occipital horns. Lysyl oxidase defect with abnormal copper use.
Type IX
