Summary
Summary Robbins Basic Pathology 9th Edition Chapter 2
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Hoofdstuk 2Inflammation is a defensive host response to foreign invaders and necrotic tissue,
but it is itself capable of causing tissue damage. The main components of
inflammation are a vascular reaction and a cellular response; both are activated by
mediators derived from plasma proteins and various cells. The cells and molecules
of host defense, including leukocytes and plasma proteins, normally circulate in the
blood, and the goal of the inflammatory reaction is to bring them to the site of
infection or tissue damage. Inflammation can be acute or chronic. Acute
inflammation is rapid in onset and of short duration, lasting from a few minutes to
as long as a few days, and is characterized by fluid and plasma protein exudation
and a predominantly neutrophilic leukocyte accumulation. Chronic inflammation
may be more insidious, is of longer duration (days to years), and is typified by influx
of lymphocytes and macrophages with associated vascular proliferation and fibrosis
(scarring). Inflammation is induced by chemical mediators that are produced by host
cells in response to injurious stimuli. An unfortunate side effect of the activation of
leukocytes may be damage to normal host tissues. The external manifestations of
inflammation, often called its cardinal signs, are heat (calor), redness (rubor),
swelling (tumor), pain (dolor), and loss of function (functio laesa). Inflammation is
normally controlled and self-limited.
The steps of the inflammatory response can be remembered as the five Rs: (1)
recognition of the injurious agent, (2) recruitment of leukocytes, (3) removal of the
agent, (4) regulation (control) of the response, and (5) resolution (repair). The
outcome of acute inflammation is either elimination of the noxious stimulus,
followed by decline of the reaction and repair of the damaged tissue, or persistent
injury resulting in chronic inflammation.
Acute inflammation has two major components: (1) Vascular changes: alterations
in vessel caliber resulting in increased blood flow (vasodilation) and changes in the
vessel wall that permit plasma proteins to leave the circulation (increased vascular
permeability). In addition, endothelial cells are activated, resulting in increased
adhesion of leukocytes and migration of the leukocytes through the vessel wall. (2)
Cellular events: emigration of the leukocytes from the circulation and
accumulation in the focus of injury (cellular recruitment), followed by activation of
the leukocytes, enabling them to eliminate the offending agent. The principal
, leukocytes in acute inflammation are neutrophils. Stimuli for acute inflammation:
infections, trauma, tissue necrosis, foreign bodies, immune reactions
(hypersensitivity reactions).
Phagocytes, dendritic cells and many other cells, such as epithelial cells, express
receptors that are designed to sense the presence of infectious pathogens and
substances released from dead cells. Receptors: (1) Toll-like receptor. There are
ten mammalian TLRs, which recognize products of bacteria (such as endotoxin and
bacterial DNA), viruses (such as doublestranded RNA), and other pathogens. TLRs
are located in plasma membranes and endosomes, so they are able to detect
extracellular and ingested microbes. Recognition of microbes by these receptors
activates transcription factors that stimulate the production of a number of secreted
and membrane proteins. These proteins include mediators of inflammation, antiviral
cytokines (interferons), and proteins that promote lymphocyte activation and even
more potent immune responses. (2) The inflammasome is a multi-protein
cytoplasmic complex that recognizes products of dead cells, such as uric acid and
extracellular ATP, as well as crystals and some microbial products. Triggering of the
inflammasome results in activation of an enzyme called caspase-1, which cleaves
precursor forms of the inflammatory cytokine interleukin-1β (IL-1β) into its
biologically active form .
The main vascular reactions of acute inflammation are increased blood flow
secondary to vasodilation and increased vascular permeability, both designed to
bring blood cells and proteins to sites of infection or injury. Vasodilation is induced
by chemical mediators such as histamine and is the cause of erythema and stasis of
blood flow. The microvasculature becomes more permeable, and protein-rich fluid
moves into the extravascular tissues. This causes the red cells in the flowing blood
to become more concentrated, thereby increasing blood viscosity and slowing the
circulation. These changes are reflected microscopically by numerous dilated small
vessels packed with red blood cells, called stasis. As stasis develops, leukocytes
(principally neutrophils) begin to accumulate along the vascular endothelial surface
—a process called margination. This is the first step in the journey of the leukocytes
through the vascular wall into the interstitial tissue.
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