|
Chemical Mediators
Diagram showing Sources of Arterial Emboli Diagram showing Sources of Venous Emboli Diagram showing common sites of Systemic Infarction from Arterial Emboli |
|
Wound healing is a complex but orderly phenomenon involving many processes: (i) Induction of an acute inflammatory process by the initial injury. (ii) Regeneration of parenchymal cells. (iii) Migration and proliferation of both parenchymal and connective tissue cells (iv) Synthesis of extra-cellular matrix proteins. (v) Remodeling of connective tissue and parenchymal components. (vi) Collagenization and acquisition of wound strength. Based on the proliferation capacity there are 3 types of cells: Labile cells: These cells are continuously dividing to replace the old ones. Example: Epithelium of skin, gastro-intestinal tract, urinary bladder and cells of bone marrow etc. Stable cells: These cells are normally non-multiplying but rapidly multiply in response to stimuli. Example: Liver, endocrine glands, fibroblasts, kidney, smooth muscle, endothelial cells etc. Permanent cells: These cells unable to multiply in postnatal life (after maturation). Example: Neurons, skeletal muscles, cardiac muscles. Regulation of cell proliferation: There are three ways of sending signals: 1. Autocrine cells : Respond to signaling substances secreted by themselves 2. Paracrine cells : Secrete substances that act on target cells in close proximity. 3. Endocrine cells (of endocrine organs): Produce substances (Hormones) that act on distal target cells. Healing by first intention (Primary Union): Healing of a clean surgical approximated incision (first intention) involves an orchestrated sequence of events as follows: 0 hours: The incision is filled with clot. 3 to 24 hours: Neutrophils from the margin infiltrate the clot. Mitoses begin to appear in epithelial basal cells; epithelial closure takes place by 24 to 48 hours. Day 3: Neutrophils are replaced by macrophages. Granulation tissue begins to appear. Day 5: The incision space is filled with granulation tissue, neovascularization is maximal, collagen fibrils begin to appear, and epithelial proliferation is now maximal. Week 2: There is proliferation of fibroblasts and continued collagen accumulation to produce a scar. Collagen deposited early in granulation tissue is type III, which is then replaced by adult type I collagen. Collagen fibers account in large part for wound strength. Inflammation and newly formed vessels have largely disappeared. Month 2: Scar now consists of connective tissue devoid of inflammation covered by intact epidermis. Healing by second intention: Healing by second intention occurs when there is more extensive loss of tissue such as, infarction, ulceration, abscess formation, and large wounds. Abundant granulation tissue grows in from the margin to fill the defect, but at the same time the wound contracts. Thus the defect is markedly reduced from its original size. Newly formed fibroblasts are swollen and show features of smooth muscle cells hence called myofibroblasts. Myofibroblasts contribute to wound contraction. Sequence of event are as follows: Within a week: Epithelium proliferates and extends between the surface debris and underlying living tissue. New capillary loops along with fibroblasts and inflammatory cells grow into the necrotic tissue from the bottom. The new capillary loops give pink, soft and granular appearance to the wound surface and hence called ‘Granulation tissue’.
Image1 : Granulation tissue showing inflammatory cells and congested blood vessels Due to rich cellular and humoral defense they are highly resistant to infection. Newly formed fibroblasts lay down collagen fibers, which are vertically oriented at the bottom and gradually change their direction as they grow upwards and finally become parallel to the surface at the superficial part. As the granulation tissue grows the necrotic tissue is removed and the area is filled up by the granulation tissue. Second week onwards: Epithelial covering is complete but devoid of sweat glands and hair follicles. Remodeling continues for many months. Factors influencing wound healing: Local factors : Example: - Infection may delay healing. - Movement of the part delays healing. - Foreign bodies may impede healing. - Size, location and type of the wound may influence healing. Systemic factors : Example: - Nutritional (protein malnutrition and vitamin C intake), - Metabolic (diabetes mellitus), and - Endocrine: Hormone (glucocorticoid therapy) hinder the inflammatory repair. Complications in wound healing: 1. Deficient scar formation: This can lead to two types of complications: (i) Wound dehiscence (ii) Ulceration 2. Excessive formation of repair components: The formation of excessive amounts of granulation tissue, which protrudes above the level of the surrounding skin and blocks re-epithelialization, has been called exuberant granulation tissue or "proud flesh". The accumulation of excessive amount of collagen may give rise to a raised tumor-like scar known as a keloid or hypertrophic scar.
Image2 : Keloid is tumour-like scar composed of abnormally large collagen fibers and large fibroblasts. 3. Formation of contractures: Contraction in the size of a wound is an important part in the normal healing. An excessive contraction, as for example in the hands or face, is called contracture. It results in deformities of the wound and the surrounding tissue, producing claw-hand or limiting the mobility of the joint.
Image3 : Claw hand Regeneration: Regeneration is the replacement of destroyed tissue by same type of tissue. Example: Liver ; Epithelium etc. It is seen in case of labile and stable cells.
Custom Search
|
|
Introduction of Pathology An outline of Diagnostic Techniques available in Pathology Diagram showing Structural Changes in Reversible and Irreversible Cell Injury Coagulation (Coagulative) necrosis Circulatory Anatomy, Physiology and Regulation Diagram showing Capillary System and Mechanisms of Edema Formation Accumulation of Glycogen, complex lipids and carbohydrates Pigments derived from Hemoproteins |