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Healing and repair
 

Healing and repair

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pathology lecture

pathology lecture

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    Healing and repair Healing and repair Presentation Transcript

    • Healing and repair - 1 Dr H.M.D.Moratuwagama Dept of Pathology Faculty of mrdicine-Ragama
    • Objectives  Describe the steps of cutaneous wound healing by primary intension and secondary intension  List the factors which delay wound healing  Describe the process of healing in specialized tissues
    • According to the potential of cell renewal 3 types of cells are present 1)Labile cells  Regenerate regularly  Surface epithelial cells  Surface epithelium of the GIT , Skin 2)Stable cells  Normally slowly regenerate  Divide when necessary  eg. Hepatocytes 3)Permanent cells  No effective regeneration  eg. Neural cells of CNS, cardiac muscle 
    • Definitions  Regeneration Growth of cells to replace the lost structure ex: skin,haemopoietic system,GIT  Healing Tissue response 1.wound 2.Inflammatory process 3.cell necrosis Two processes-Regeneration Scar formation-laying down of fibrous tissue
    • Tissue injury Partial Total Labile cells Stable cells Permanant Scar Regenerate Regenerate/scar Scar
    • Scar formation occurs when 1)Damage to permanent cells 2)Severe destruction of connective tissue frame work 3)With extensive cell injury 4)In chronic inflammation
    • Steps in repair by scar tissue formation 1)Inflammatory response  Polymorphs and macrophages  Remove damaged and dead tissue 2)Proliferation and migration of parenchymal and connective tissue cells 3)Formation of new blood vessels (angiogenesis) and granulation tissue
    • Steps in repair by scar tissue formation cont. 4) Synthesis of ECM proteins and collagen deposition 5) Tissue remodeling 6) Wound contraction 7) Wound strength
    • What is angiogenesis? Formation of blood vessels from existing blood vessels From  A) Endothelial precursor cells in BM  B) From pre-existing vessels
    • What is granulation tissue?  Highly vascularized connective tissue  Composed of – Newly formed capillaries Proliferating fibroblasts Inflammatory cells in oedematous stroma  Macro – Pink granular Soft and fleshy
    •  new capillaries (result of proliferation of endothelial cells - angiogenesis or neovascularization) in an edematous atmosphere of fibroblasts (spindle shaped), myofibroblasts, mononuclear inflammatory cells, macrophages, neutrophils,
    • Growth factors involved in angiogenesis 1)Formation of new vessels  VEGF  FGF 2)Stability of new vessels  Angiopoietin 1 & 2 - Periendothelial cells  PDGF - Smooth muscle cells  TGF – beta - ECM protein secretion
    • ECM protein production (Initial)  VEGF - (Angiogenesis and ) increased vascular permeability Exudation and deposition of plasma proteins Provides a stroma for the proliferating endothelial cells and fibroblasts
    • ECM protein production Fibroblasts migration  Macrophages Growth factors  TGF – beta  PDGF  FGF , platelets , endothelium Cytokines TNF , IL -1 Fibroblast migration and proliferation
    • ECM deposition and scar formation  Growth factors (PDGF , FGF , TGF) & Cytokines (IL-1 & IL-13)  Stimulate  Net fibroblast to produce collagen collagen is dependant on both the production and degradation
    • Tissue remodeling  Degradation of collagen and other ECM proteins by a family of matrix metalloprotinases (MMPs)  TIMs –(Tissue inhibitors of metaloprotinases) inhibit their action  Net result is the formation of an avascular firm white scar tissue
    • Wound contraction  By the contraction of a specialized cell in the granulation tissue called myofibroblasts  Wound defect decreased in size  Harmful effect – Stenosis , contractures
    • Wound strength It is acquired by 1) Increase collagen deposition 2) Cross linking of collagen fibers 3) Change of collagen fibers from type 3 to type 1
    • Cutaneous wound healing 1)Inflammation  Early and late 2)Granulation tissue formation and re-epithelialization 3)Wound contraction ECM deposition and remodeling
    • Wound healing 1)Healing by first intension (Primary union)  -wounds with opposed edges2)Healing by second intension (Secondary union)  -Wounds with separated edges-
    • Healing by first intension (Primary union)  In –Surgically incised Clean and uninfected Limited death of epithelial cells and connective tissue Edges approximated by surgical sutures
    • Healing by second intension Wounds with  Extensive cell death  Large defects +/infection  Wounds not approximated by sutures
    • Healing by primary intension  Surgical  Gap wounds filled by clotted blood containing fibrin and blood cells  Scab forms
    • Healing process Within 24 hrs  Neutrophils enter 24-48hrs  Epithelial cells move and fuse in the midline Day 3  Macrophages move in  Granulation tissue forms  Collagen laid down  epithelial cell layer forms
    • Day 5  Granuation tissue fills the gap  Maximal neovascularization  Collagen fibrils increases  Epithelial cells thickens 2nd Week  Accumulation of collagen and fibroblast proliferation  Regression of vascular channels, inflammation and oedema 4th Week  Scar  Covered by epidermis  Dermal appendages are absent  Wound strength - over several months
    • Differences from primary union 1) Larger fibrin clot 2) More necrotic debris and exudate 3) Intense inflammatory reaction 4) Abundant granulation tissue 5) Wound contraction (by myofibroblasts) 6) Scar formation and thinning of epidermis
    • Primary wound healing
    • Secondary Wound Healing
    • Secondary Wound Healing
    • Secondary Wound Healing
    • Wound strength  Day 7 10% of the original tissue  2nd to 3rd month 70-80% of original tissue
    • Factors that retard wound healing Local factors Poor blood supply - arteriosclerosis, venous abnormalities(ex: varicose veins)  Denervation  Local infection  Foreign bodies – interfere with healing and cause infection  Presence of a haematoma  Mechanical stress  Presence of a necrotic tissue 
    • Systemic factors that delay wound healing  Anaemia  Drugs-Steroids ( anti-inflammatory) , cytotoxic drugs  Genetic disorders with collagen defects Ehlers – Danlos syndrome Osteogenesis imperfecta Marfans syndrome  Diabetes  Malignancy
    • Systemic factors that delay wound healing cont.  Nutritional deficiencies – eg- Protein, Vitamin C, Zinc  Systemic infection  Trauma , hypovolaemia , hypoxia  Uraemia  Haematological abnormalities – Defect of neutrophil function
    • Other factors that influence wound healing  Age  Size  Location  Mechanical factors
    • Summary  The process by which healing occurs in a tissue is dependant on several factors – Type of cell , extent of injury etc  Depending on the type of wounds, healing process follows two pathways - Healing by primary intension - Healing by second intension  There are systemic and local factors that may delay wound healing
    • THANK YOU