Body Response To Tissue Damage: Healing And Repair Flashcards
Wound healing 2
Day 2
Late inflammation
Macrophages begin to infiltrate incisional space and demolish fibrin
Surface continuity is re-established in a thin surface layer
Stages of wound healing 1)
Neutrophils appear at the margins of the incision
Acute inflammatory response-> platelets-> Chemokines
Swelling pain and redness
Exudate neutralises damage and initiates organisation
Epithelial cells undergo mitosis and migrate across wound
Initial vasoconstriction the vasodilation via prostaglandins, thrombin
Fibrin initiates coagulation
Wound healing 3
Day 3
Granulation tissue begins to invade tissue space
Fibroblasts lay down collagen
Surface continuity is reinforced by thickening of epithelial layer
Wound healing 4
Day 5
Incisional space filled with vascular granulation tissue
Collagen is deposited
Surface epithelial becomes normal thickness
Acute inflammatory response is reduced
Wound healing 5
Day 7
Wound has 10% of tensile strength
Remove sutures
Wound healing 6
Day 10
Further fibroblast proliferation and collagen deposition
Adds strength to the wound
Wound healing 7
Day 15
Collagen deposition follows the lines of tissue stress
Granulation tissue looses some vascularity
Wound healing 8
Wound has 50% of tensile strength
Wound healing 9
3 months
Wound achieves 80% of tensile strength
Only marginally more vascular than normal skin-> removed in coming months to become white
Remodelling occurs
Five key events in wound healing
Angiogenesis-> local vessels form-> basic fibroblast growth factor
Mitogenesis-> divide to form fibroblasts and myoblasts-> platelet derived and basic fibroblast growth factor
Chemotaxis and motility-> migration-> platelet derived and basic growth factor
Fibrogensis-> secrete collagen-> transforming growth factor, IL-1, tumour necrosis factor
Remodelling-> collagen degrading enzymes produced
Adverse effects of acute inflammation
May cause the symptoms
-> meningitis, croup/diphtheria, pericarditis, pleurisy, peritonitis
Pleurisy-> painful because exudate is fibrinous
Meningitis-> Purulent exudate fills space in the pia-> raised intracranial pressure-> microthrombosis in small vessels
Adverse effects of chronic inflammation/scars
Chronic inflammation always heals by a scar
Scars are functionless
Strong but not-> elastic, contractile, secretory, absorptive or pretty
Factors leading to inadequate healing
Continuing infection Foreign or uncleared necrotic material Ischaemia Diabetes Denervation Steroid therapy Previous irradiation
Healing of brain necrosis or infarction
Brain parenchyma doesn’t contain fibroblasts-> can’t make collagen
Instead undergoes liquification
Phagocytosis-> following cell death removal of damaged cells by phagocytotic resident microglial cells, supplemented by monocytes from the blood
Gliosis-> astrocytes become activated-> proliferate to fulfil metabolic roles in protecting neurones
Damaged areas replaced by astrocyte proliferation-> glial scar
Bone healing
Collagenous scar isn’t strong enough
Bone needs to be replaced by bone