Pathophisiology 21 - Grade: 5 PDF

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21. Inflammation – definition and biologic significance. Etiology and pathogenesis. Classification and outcome of inflammation. Cardinal clinical signs of inflammation. DEFINTION: a protective response to eliminate the initial cause of injury and deal with the consequences of cell injury i.e. clearing dead cells. Part of the body becomes reddened, swollen, hot, and often painful, especially as a non-specific reaction to injury or infection. It’s a body defense reaction. BIOLOGICAL SIGNIFICANCE OF INFLAMMATION The purpose of inflammation is to bring fluid, proteins, and cells from the blood into the damaged tissues. Tissues are normally bathed in a watery fluid (extracellular lymph) that lacks most of the proteins and cells that are present in blood, since the majority of proteins are too large to cross the blood vessel endothelium. Thus there have to be mechanisms that allow cells and proteins to gain access to extravascular sites where and when they are needed if damage and infection has occured. The main features of the inflammatory response are, therefore: vasodilation, i.e. widening of the blood vessels to increase the blood flow to the infected area; increased vascular permeability, which allows diffusible components to enter the site; cellular infiltration by chemotaxis, or the directed movement of inflammatory cells through the walls of blood vessels into the site of injury; changes in biosynthetic, metabolic, and catabolic profiles of many organs; and activation of cells of the immune system as well as of complex enzymatic systems of blood plasma. Of course, the degree to which these occur is normally proportional to the severity of the injury and the extent of infection. CARDINAL CLINICAL SIGNS OF INFLAMMATION: RUBOR : redness (due to dilating blood vessels) TUMOR : swelling (leakage of plasma fluid and proteins from BV to tissue) CALOR : heat (due to the inflammatory response the dilating blood vessels) DOLOR : pain (sensory nerve fibers, mechanical damage and prostaglandins action) FUNCTIO LAESAE : loss of function (if chronic) ETIOLOGY: Exogenous Endogenous Biologic factors (bacteria) Physical factors (radiation) Chemical factors (acid attack) Mechanical factors (car accident) Hypoxia (NO released from endothelial cells – powerful vasodilator to increase blood flow) Secretions (acid, Bile, Urea, Uric acid) Depositions (Salts, Toxic compounds Immune complexes) Immune reaction CLASSIFICATION: Inflammation may be Acute or chronic, specific or non-specific. According to tissue response, it may be Normoergic, Hyperergic and Hypoergic inflammation. The Normoergic= adequate reaction of organism. Hyperergic= disproportionally strong reaction of organism. Hypoergic = insignificant changes in tissues. Acute inflammation: the pathological agent is destroyed completely and the process ends in settling of the inflammation and reparation (restoration to original condition, healing with consequences, abscess/phlegmon formation), Cold and flu, other minor infections. Chronic inflammation: develops as the result of persistent influence of the pathological agent on an organism, organ, and tissue, which cannot be destroyed and eliminated by the organism. Leads to fibrosis, i.e. liver Cirrhosis, chronic pancreatitis, PATHOGENESIS: It develops through the following phases. 1. Alteration: Cell damage cytokines cause mast cells to release histamine vasodilation increased blood flow 2. Transudation: if inflammation is not severe, only fluids and small proteins enter the interstitium as the endothelial spaces are not so large. 3. Exudation: if inflammation is severe, larger proteins such as fibrin as well as RBCs and complement proteins enter. 4. Emigration: Neutrophils enter by diapedesis 5. Proliferation: If the vessel is damaged, fibrinogen and fibronectin are deposited at the site of injury. Chronic inflammation: If the damage is sufficiently severe, a chronic cellular response may follow over the next few days. A characteristic of this phase of inflammation is the appearance of a mononuclear cell infiltrate composed of macrophages and lymphocytes. The macrophages are involved in microbial killing, in clearing up cellular and tissue debris, and they also seem to be very important in re-modelling the tissues. Neutrophils- bacterial infections, Lymphocytes- viral infections, Eosinophils- parasitic infections OUTCOME: Over the next few weeks, resolution may occur, meaning that the normal tissue

architecture is restored. Blood clots are removed by fibrinolysis, and if it is not possible to return the tissue to its original form, scarring results from in-filling with fibroblasts, collagen, and new endothelial cells. Generally, by this time, any infection will have been overcome. However, if it has not been possible to destroy the infectious agents or to remove all of the products that have accumulated at the site completely, they are walled off from the surrounding tissue in granulomatous tissue. A granuloma is formed when macrophages and lymphocytes accumulate around material that has not been eliminated, together with epitheloid cells and gigant cells (perhaps derived from macrophages) that appear later, to form a ball of cell....