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Inflammation is the body's mechanism for coping with agents that could damage it. In other words, inflammation is a protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces. Although the processes of acute and chronic inflammation are an important protective mechanism used by the body to deal with potentially damaging agents, they are potentially damaging to the body and must be closely regulated. The basic steps in acute inflammation allow white blood cells to move from the blood to the tissue location where they are required. Acute inflammation can resolve completely if the inciting agent is removed, or it can have one of several other sequelae, including chronic inflammation. This chapter will discuss general concepts of acute and chronic inflammation, specific features of acute inflammation (including cardinal signs, causes, steps, and morphology and outcomes), specific features of chronic inflammation, and repair.

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General Concepts of Acute and Chronic Inflammation

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Overview: The body must undergo changes locally through vasodilation and increased vascular permeability in the area of the agent inciting the inflammatory reaction to allow white blood cells to accumulate. The white blood cells must then leave the blood vessel, cross the basement membrane, and be drawn to the area where they are needed. The process by which white blood cells are drawn to the area where they are needed is referred to as chemotaxis. Acute inflammation has a rapid onset, lasts for minutes to days, and is characterized by exudation of fluid and protein from vessels and emigration of neutrophils. Acute inflammation is a protective process that is designed to rid the body of the inciting agent and set up the process of repair. Chronic inflammation has a longer time course (days to years) and involves different cell types than does acute inflammation (lymphocytes and macrophages versus neutrophils). Also, in chronic inflammation, tissue repair coexists with tissue destruction.

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Cardinal signs of acute inflammation: Rubor (red discoloration), calor (heat), dolor (pain), tumor (mass effect), and loss of function.

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Causes of acute inflammation: Infection, trauma, physical and chemical agents, necrosis, foreign bodies, and immune reactions.

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Stages of acute inflammation (Table 2-1)

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  1. Vasodilation (after a transient vasoconstriction)

    • How: Vasodilation occurs through release of mediators from cells. These mediators include histamine, prostacyclin (PGI2), and nitric oxide (NO).
    • Why: Vasodilation increases the hydrostatic pressure by causing slowing (sludging) of blood flow. Sludging of blood also causes margination of leukocytes along the wall of the blood vessel.

  2. Increased vascular permeability (increased leakiness of vessels)

    • How: Increased vascular permeability occurs through release of mediators from cells. These mediators include histamine and leukotrienes C4, D4, and E4.
    • Why: Increased vascular permeability allows fluid to cross into the interstitial tissue, which increases protein levels in the interstitial tissue, thereby decreasing osmotic pressure in the blood ...

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