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Lecture 2

PATHO lecture 2 Inflammation and tissue repair.docx

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Department
Nursing
Course Code
NURS 2090
Professor
Nikki Kelly

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PATHO lecture 2 Inflammation and tissue repair 5) In this lecture we will be discussing two types of inflammation: acute inflammation: the body’s normal response to injury and chronic inflammation: the body’s altered response to unrelenting injury. 9) This requires the response of a blood vessel near the site of the injury. The blood vessel must widen or dilate to increase blood flow at the site of injury and the lining of the blood vessels become more permeable as a result of loosening the basement membrane of the blood vessels and adjacent endothelial cells. The blood is composed of cells active in phagocytosis for removing harmful agents and cells that promote healing and repair and increased fluid dilutes harmful substances . . . . All of this is orchestrated by inflammatory mediators which are located in the blood plasma and in cells such as platelets, endothelial cells, monocytes, and macrophages . .. Must be constantly ready to act anywhere in the body. 11) One of the most important white blood cells is the mast cells in the connective tissue and near all blood vessels . .. They are like emergency first responders . . .responsible for the production and immediate release of inflammatory mediators through degranulation .... Breaks apart and releases them; basophils do the same thing. Some inflammatory mediators include histamine, leukotrienes and prostaglandins. Platelets release IM to promote vasodilation, clotting, attraction of WBCs and healing of injured tissue. Serotonin increases vasodilation and increased vascular permeability. Damaged epithelial cells can release platelet activating factor which is a complex lipid stored in the cell membrane with key roles in vasodilation, clotting and attracting WBCs to the site of injury. Another example is arachidonic acid derived from the plasma membrane of the injured cell which generates various inflammatory mediators such as prostaglandins, leukotrienes and thromboxane. They are active in vasodilation and vasoconstriction, bronchodilation and bronchoconstriction and attraction of leukocytes. Corticosteriods work to block a conversion. Plasma derived: inflammatory mediators are constantly circulating within the plasma The pathways are responsible for activation and deactivation of the inflammation response; in other words the regulation. Multiple pathways are need. Complement system are several proteins that comprise 10-15% of the plasma; produced in liver and triggered by the presence of microorganisms . . . Release a cascade of inflammatory mediators and the primary role is to destroy and remove microbes to prevent infection through opsonization (making bacteria vulnerable to phagocytosis) and cell lysis. The clotting pathway promotes coagulation through a cascade of clotting factors and suppresses when clotting is complete and various clotting factors produce and release inflammatory mediators . . . And the kinin pathway: highly potent vasoactive inflammatory response and amplifies the inflammatory response by triggering other Ims. So the steps are: tissue injury, blood vessel vasodilation, increased vascular permeability, activation of clotting cascade, continued release and circulation of IM 16) Chemotaxis: process of moving certain cells to the site of injury using chemotactic factors (i.e. The neutrophil one attracts neutrophils etc). Cellular adherence: attraction and binding regulated by chemotactic factors by endothelial cells, receptors that bind leukocytes to the surface of endothelial cells near the site of injury Cellular migration: migrate or move across endothelial cells to get to the source of injury in a process called diapedesis. 28) Persistent or recurring state of inflammation (an unrelenting injury, persistent infectious process or autoimmune condition). Longer lasting actions of monocytes, macrophages and lymphocytes . .. Producing proteinases that destroy elastin and other tissue components. These enzymes break down dead tissues but they do not discriminate. Fibroblasts active in chronic inflammation . . .collagen development, and extensive scarring . . Permanent loss of function or scarring. In some cases, chronic inflammation results in granuloma formation which is regulated by macrophages. Granuloma forms when injury too difficult to control by usual inflammatory and immune mechanisms (TB). By forming granulomas, macrophages protect healthy unaffected tissue . . Giant cells engulf particles and epithelioid cells gather and contain smaller substances by forming a wall or fibrotic granuloma. .. . Necrosis inside . . . Necrosis goes through the wall and fibrotic capsule remains. 29) Infection will be caused by microorganisms and ulceration from poor perfusion . . Open crater like lesions . . Dehiscence a problem of deficient scar formation in which the wound splits or bursts open . . Invasion of microorganisms. Mechanical stress. . . Poor development of extracellular matrix and ineffective or inadequate collagen. Keloids . . Hypertrophic scars that result from excessive collagen production at the site of injury . . . Adhesions problem with collagen deposition. Collagen fibers can develop and form adhesions with injuries located in or near
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