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| − | ==Introduction==
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| − | * Acute inflammation is characterised sudden onset and may last for a few hours to a few days.
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| − | * Vascular, humoral and cellular alterations cause the 5 cardinal signs as a result of exposure of tissues to various causes.
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| − | * Acute inflammation can:
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| − | *# Be fatal
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| − | *# Resolve by regeneration in association with the host defence mechanisms.
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| − | *#* May be assisted by therapeutic measures.
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| − | *# Undergo repair by fibrosis.
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| − | *# Become chronic.
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| − | *#* First goes through a subacute phase.
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| − | *#* Is dependent upon the persistence of the agent and the amount of damage caused.
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| − | ==Sequence of Events==
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| − | * The following sequence of events is provoked by the presence of the irritant.
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| − | # '''Momentary vasoconstriction'''
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| − | #* Following contact with the irritant, there is momentary vasoconstriction of the blood vessels in the affected area.
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| − | #* This is reversed within minutes.
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| − | # '''Dilation of the blood vessels'''
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| − | #* Initially, dilation of the capillaries is caused by the release of chemical mediators.
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| − | #* Arterioles then dilate under the influence of a local axon reflex.
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| − | #* This gives rise to an initial acceleration of the blood flow to the area.
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| − | #** This later gives way to a slowing of blood flow, caused by alterations in vascular endothelial permeability and the filling of previously closed capillaries.
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| − | # '''Exudation of fluid'''
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| − | #* Follwing the slowing of blood flow and altered capillary permeability, a protein-rich fluid is exudated.
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| − | # '''Margination of leukocytes'''
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| − | #* Circulating white blood cells are attracted to the altered endothelial surfaces.
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| − | # '''Emigration of leukocytes'''
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| − | #* [[Leukocytes|Leukocytes]] migrate through the altered endothelium to reach the injured area.
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| − | #* This is an active process - [http://www.cellsalive.com/chemotx.htm| chemotaxis].
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| − | #** The cells are attracted to the endothelium by release of proteins, and further into the tissues by factors released from cells in the damaged area.
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| − | #** The emigrated leukocytes and components of the fluid exudate are also chemotactic.
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| − | #** More cells and fluid are attracted to the area.
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| − | # '''Emigration of red blood cells'''
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| − | #* [[Erythrocytes|Erythrocytes]] migrate through the gaps in the altered endothelium to the damaged tissue.
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| − | # '''Induction of an increase in temperature'''
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| − | #* This may occur either locally or systemically.
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| − | #* A systemic rise in temperature is known as pyrexia.
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| − | #** Occurs in generalise acute inflammation.
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| − | #** Pyrogens act on the temperature control centres in the hypothalamus, and are released from:
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| − | #*** [[Neutrophils|Neutrophils]], [[Eosinophils|eosinophils]] and [[Macrophages|macrophages]]
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| − | #**** Particulary [[Neutrophils|neutrophils]] when they begin to phagocytose.
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| − | #*** The cellular coat of gram-negative organisms.
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| − | #*** Necrosis of damaged tissue cells.
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| − | #*** Antigen-antibody complexes.
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| − | #*** Tumours.
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| − | #**** Particularly those which have metastasised
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| − | #**** It may be difficult to separate this from the pyrexia caused by the central necrosis in such tumours.
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| | *** The very end result is a fibrous scar. | | *** The very end result is a fibrous scar. |
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| − | ==Cells==
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| − | * The classical cells of acute inflammation are [[Neutrophils|neutrophils]], [[Eosinophils|eosinophils]], [[Macrophages|macrophages]], [[Mast Cells|mast cells]] and [[Basophils|basophils]].
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| − | ** [[Macrophages|Macrophages]] are a common feature of acute and chronic inflammation.
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| | [[Category:Inflammation]] | | [[Category:Inflammation]] |