Inflammation: Causes and Purpose

Study Notes

Inflammation is a protective response aimed at eliminating the initial cause of cell injury, as well as necrotic cells and tissues resulting from the original injury.

Exogenous causes: trauma, surgery, infection, caustic chemicals, extremes of heat or cold, immune responses
Endogenous causes: ischemic damage

Inflammation is a process involving multiple cellular, humoral, and tissue participants
Inflammation occurs only in living tissue, cannot occur in dead tissue
Inflammation is a series of events that form a continuum, a defensive reaction that always requires an irritating stimulus

Acute inflammation: rapid in onset, short duration, characterized by exudation of fluid and plasma proteins, and emigration of leukocytes, predominantly neutrophils
Chronic inflammation: longer duration, associated with the presence of lymphocytes and macrophages, proliferation of blood vessels, fibrosis, and tissue injury

Mild reactions: little or no tissue destruction, slight evidence of vascular involvement, and little exudation
Moderate reactions: some damage to host tissue, easily visible host reaction to the injury, leukocytic accumulation, and vascular phenomena
Severe reactions: considerable tissue damage, abundant exudation

All inflammatory reactions have a beginning, and most have an end
In between lies a variable span of time in which the character of the evolving reaction can change

Neutrophils: first leukocytes to gather at sites of acute inflammation, constitute the cellular defense system against bacteria, participate in phagocytosis, and release lytic lysosomal enzymes
Eosinophils: abundant at sites of inflammation in diseases of immunologic or allergic origin, respond to antigen-antibody complexes
Basophils and mast cells: release heparin and histamine in response to antigen-antibody complexes
Monocytes and macrophages: originate from circulating monocytes, larger than neutrophils, possess gray-blue cytoplasm, participate in phagocytosis, and contain phagocytic inclusions

Heat (increase in temperature) caused by increased blood flow
Pain caused by irritation of nerve endings by chemical mediators
Swelling of tissue caused by vascular dilatation and accumulation of inflammatory fluid and cellular exudate
Redness of tissue caused by vascular dilatation
Loss of movements or function due to pain and tissue damage

Alterations in vascular caliber that lead to an increase in blood flow (vasodilatation)
Structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation (increased vascular permeability)
Emigration of leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent

Changes in vascular flow and caliber begin early after injury and develop at varying rates depending on the severity of the injury
Vasodilation is one of the earliest manifestations of acute inflammation, induced by the action of several mediators, notably histamine and nitric oxide

Histamine: released from mast cells, increases blood flow to the area, and leakage of fluid and proteins from the blood into the tissue space
Nitric oxide: produced by endothelial cells and macrophages, causes smooth muscle relaxation in the vessel wall, and reduces platelet activation and aggregation