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Published byAngela Webb Modified over 9 years ago
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Repair
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* Definition: Replacement of damaged tissue with new healthy living tissue.
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* Types of the cells according to the power of cell division: 1. Labile cells: 1. Labile cells: are contentiously dividing cells and renew themselves: e.g. skin epithelium, mucosal lining of the GIT, haematopoietic cells (blood cells ). 2. Quiescent cells (Stable): 2. Quiescent cells (Stable): cells divide when there is a need e.g. liver, kidney and pancreas.
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3. Permanent cells: 3. Permanent cells: Non-dividing cells so when injured heal by fibrous tissue or glial tissue (in CNS only) e.g. nerve cells and skeletal, cardiac muscle cells.
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* Types of repair: A. Regeneration: Replacement of the damaged cells by new healthy cells of the same type. Done by proliferation of the adjacent healthy cells. Occurs with minor damage of labile cells and stable cells. Examples: mild liver injuries and bone fractures
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B. Fibrosis or gliosis: Replacement of the damaged tissue by fibrous tissue or glial tissue (in CNS). Occurs in the healing process of permanent cells or in stable cells with marked damage. Examples: 1.Myocardial infraction: heal by fibrosis. 2.Cerebral infarction. Heal by gliosis.
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Wound Healing Cutaneous wound healing is generally divided into 4 phases: 1.Hemostasis. 2.Inflammation. 3.Granulation tissue formation and Re- epithelialization 4.Fibrous tissue formation and remodeling.
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1. Homeostasis Immediately after injury the cut vessels bleed inside the wound defect to form a blood clot that unit the two cut ends temporarily. Vasoconstriction of the injured vessels at the edges of the wound followed by platelets aggregation and adherence to the damaged endothelium. Stimulation of coagulation system will form fibrin. Fibrin network is formed over the aggregated platelets to form a homeostatic plug that stops bleeding inside the wound.
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2. Inflammation Mediated by polymorphs and macrophages. Within the first 6-8 hours, the polymorphonuclear leukocytes (PMNs) kill any organism in the wound and liquefy any necrotic debris. As the process continues, monocytes also exude from the blood vessels. These are termed macrophages. The macrophages continue and engulf the necrotic debris.
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3. Granulation tissue formation and re- epithelization In days 5-7, fibroblasts migrate into the wound. Angiogenesis is the formation of new capillaries from the healthy blood vessels at the edge of the wound. These new capillaries fill the wound defect and surrounded by fibroblasts.
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The newly formed capillaries + fibroblasts = granulation tissue. Re-epithelization occurs by proliferation and migration of the healthy epidermal cells from the edges of the wound inwards.
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Granulation tissue
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capillary fibroblast
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4. Fibrous tissue formation and remodeling After the third week, fibroblasts lay down collagen fibers types I and III. Excess collagen is degraded by collagenase enzyme which secreted from macrophages in a controlled manner (remodelling).
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* Wound contraction: Is a process done by myofibroblasts (modified fibrobalsts), which resemble contractile smooth muscle cells. This occurs to give the healing wound more strength.
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* Types of wound healing: 1. Healing by primary union: -Occurs with clean, non-gaping wounds (stitched surgical incision). -The result scar is small, thin, regular and flat. 2. Healing by secondary union: - Occurs with extensive tissue loss as in: large wounds, infected wounds, abscess, ulcers….etc. - The resulting scar is large, thick, irregular and elevated.
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* Complications of wound healing: 1. Ulcers: 1. Ulcers: discontinuity of the covering epithelium or mucous membrane. 2. Sinus: 2. Sinus: is blind end track of septic granulation tissue connecting a cavity to the outside e.g. pilonidal sinus 3. Fistula: 3. Fistula: is a tract of septic granulation tissue connecting 2 epithelial surfaces e.g. perianal fistula. 4. Weak atrophic scar: 4. Weak atrophic scar: this may lead to hernia.
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5. Hypertrophied scar. Large sized scar that don’t grow beyond the boundaries of the original wound. 6. Keloid formation: Large sized scar that grow beyond the boundaries of the original wound and even infiltrating the surrounding tissue.
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Its periphery shows claw-like extensions. Occurs due to overproduction of collagen or defect in its degradation. Affect certain genetically predisposed persons. Radiotherapy is curative.
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Hypertrophic scar Keloid
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A B
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* Factors affecting Repair: I. Local factors : The type of the damaged cells (labile, stable or permanent). Severity of the damage. Presence of foreign body. Presence of necrotic tissue. Infection. Irradiation. Blood supply.
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II. General factors: Age of patient. Nutrition status. Diseases: Diabetes, malignancy, anaemia. Drugs: Corticosteroid therapy, chemotherapy..
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