Acute and Chronic Inflammation
Dr. Eric Po Lasala,
DPSP
Acute Inflammation
n It is an immediate and early response to injury
n It destroys, dilute or wall off the injurious agent
n It acts into motion a series of events that as far as possible, heal and reconstitute the damaged tissue
n It is a fundamental protective response
n Its goal:
o To rid the body of the initial cause of cell injury
o To prepare the body for the consequences of the injury
n It is usually of short duration lasting from several minutes, hours or days
n Its main characteristics:
o Exudation of fluid and plasma proteins (edema)
o Emigration of leucocytes (neutrophils)
5 Cardinal Signs of Inflammation
n Rubor - redness
o Brought about by the presence of vasodilatation which occurs seconds after the first injury
n Tumor - swelling, or mass
o Brought about by the exudation of plasma tissue fluids which accumulate around the site of injury
n Calor - heat
o Associated with the presence of vasodilation which occurs initially thus increasing the heat dissipation in the area of injury
n Dolor - pain
o The initial and subsequent responses of the cells and the different proteins that interact in the presence of injury will release a multitude of mediators that cause pain
n Functio laesa - loss of function
o In the presence of all the four ( rubor, tumor, calor, and dolor ) other characteristics of inflammation overall effects lead to the loss of function of the injured site
3 Major Components of Acute Injury
n Increased blood flow- this is brought about by the alteration in the caliber of the blood vessels
n Structural changes-mostly of the small blood vessels that promotes the exudation of plasma and leucocytes
n Immigration of leucocytes towards the site of injury
Exudate
n This is brought about by the escape of fluid, proteins and blood cells from the vascular system into the interstitial tissues and body cavities
n Characteristics of an exudate:
o High protein concentration, from the soluble plasma proteins and the cellular debris components
o Specific gravity of > 1.020
o Signifies an abnormal permeability of the small blood vessels in the sites involved
Transudate
n Another type of fluid accumulation but with a different mechanism, usually as a result of imbalance in the hydrostatic pressure across the endothelial cells
n The fluid is of low protein content, mostly albumin
n Specific gravity of < 1.020
Vascular Changes in Acute Inflammation
n Vasoconstriction - this is the first and most immediate change in injury
o It is transient
o Usually involves the arterioles
o Lasts for only a few seconds
n Vasodilation - usually as a result of the arteriolar dilatation and opening of the capillary bed
o Initially results to an increase in the blood flow to the injured area
n Stasis - results from the increased permeability of the vasculature
o Gives rise to the exodus of protein rich fluids to the interstitial spaces
o The resulting transfer of plasma protein into the interstitial spaces will increase its oncotic pressure, thereby pulling more fluid from the vasculature
Mechanisms of Increased Vascular Permeability in Inflammation
n Endothelial Contraction
o This gives way to widened endothelial junctions where not only fluid and protein can pass but also cells
n Cytoskeletal Reorganization
o This will reshape the endothelial cells leaving spaces between cells
n Direct injury to the endothelial cells
o Subsequent loss of endothelial cells leaves a gap for fluid and cells to pass
n Leucocyte Dependent Injury
o Activated leucocytes containing toxic intracellular substances can digest the injured endothelial cells creating a space in the endothelial system
n Increased Transcytosis
o Transcytosis is promoted by injurious agents allowing the endothelial cells to form more intracellular channels for the intravascular substance to pass through it
o The cellular channels may coalesce to form larger channels allowing leucocytes to pass
Leucocyte Activity in Acute Inflammation
n Rolling
u After an injury, the leucocytes which are normally flowing peripherally and smoothly along the microvasculature tend to bump into the endothelial wall and come into close contact with the endothelial cells as it travels through the system
n Activation
u The release of chemical mediators as a result of the injury results to the activation of the leucocytes and the endothelial cells at the same time
n Adhesion
u The leucocytes tend to become more adherent to each other as result of the different chemical mediators released into the plasma
n Pavementing
u The leucocytes will also become more adherent to the walls endothelial cells, and side by side, they will give the appearance of a pavement pattern
n Transmigration
u Through the injured endothelial walls, the leucocytes that has been activated finds its way out of the vascular channels and to the source of the injury
n Chemotaxis
u The leucocytes are then attracted to the source of the injury by the actions of chemical agents that also activated them
u The leucocytes that finds the source of injury will release enzymes that are harmful to the injurious agent and the host
n Phagocytosis
u The activated leucocytes engulf the injurious agent and at the same time release protease enzymes and other metabolites which serve as chemoattractants to other leucocytes and also harmful to the injurious agent
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Chronic Inflammation
n Any inflammation of prolonged duration, usually from weeks to months
n Histologically associated with the presence of:
o Lymphocytes
o Macrophages
o Neovascularization
o Fibrosis
o Tissue necrosis
n There are three processes simultaneously occurring during a chronic inflammation:
o The inflammation
o Tissue destruction
o Repair of the injured tissues
n Settings in which a chronic inflammation may set in:
o Persistent infections by certain organisms
« Tuberculosis
« Fungal infections
« Syphilis
n Settings in which a chronic inflammation may set in:
o Prolonged exposure to potentially toxic agents
« Silica
« Atheromatous plaques
n Settings in which a chronic inflammation may set in:
o Autoimmunity
« When a host’s own immune system is activated against itself
« This will lead to a series of destructive events that will cause debilitating disease
n Characteristics of a Chronic Inflammation:
o Infiltration of mononuclear cells
o Tissue destruction
o Attempts of repair
Granulomatous Inflammation
n A type of chronic inflammation
n Predominant cell types seen:
u Epitheloid cells (activated tissue macrophages)
n Classic example- Tuberculosis
n Granuloma -is a mass of chronic inflammatory cells made of epitheloid cells, lymphocytes, multinucleated Langhan’s Giant cells and the characteristic caseous necrosis which is the end result of the destructive effects of all the inflammatory cells combined
Pathway to the Mechanism of Fever
Outcome of Inflammation
n Acute Inflammation:
o Resolution
o Abscess formation
o Healing and Fibrosis
n Chronic Inflammation
o Regeneration
o Scarring or Fibrosis