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When acute inflammation becomes over-active it can be fatal. A classic example is septic shock caused by bacterial LPS. In most cases though acute inflammation acts to protect and repair the damage to the tissue by resolving by regeneration in association with the host defence mechanisms. To assist in resolving and controlling inflammation therapeutic measures have been developed, with some being very recognisable therapies, for example the Non-Steriodal Anti-Inflammatory Drugs (NSAIDs e.g. Aspirin and Ibuprofen N.B. NOT paracetomal).

When acute inflammation becomes over-active it can be fatal. A classic example is septic shock caused by bacterial LPS. In most cases though acute inflammation acts to protect and repair the damage to the tissue by resolving by regeneration in association with the host defence mechanisms. To assist in resolving and controlling inflammation therapeutic measures have been developed, with some being very recognisable therapies, for example the Non-Steriodal Anti-Inflammatory Drugs (NSAIDs e.g. Aspirin and Ibuprofen N.B. NOT paracetamol).

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#* Circulating white blood cells, in particular [[Neutrophils|neutrophils]], begin adherence to the altered endothelial surfaces.

#* Circulating white blood cells, in particular [[Neutrophils|neutrophils]], begin adherence to the altered endothelial surfaces.

# '''Emigration of leukocytes'''

# '''Emigration of leukocytes'''

#* [[Leukocytes|Leukocytes]] migrate, by an active process, through the altered endothelium to reach the injured area. This process is called '''diapedesis'''. The cells are stimulated to do this by chemoattractants in the vicinity of the injury, for example the [[Cytokines|cytokines]] TNF-.

#* [[Leukocytes|Leukocytes]], again mostly neutrophils, migrate, by an active process, through the altered endothelium to reach the injured area. This process is called '''diapedesis'''. The cells are stimulated to do this by chemoattractants in the vicinity of the injury, for example the [[Cytokines|cytokines]] TNF-α, Il-1 and IL-6, and the [[Complement|complement]] components C3a and C5a. Once through the endothelium, emigrated leukocytes and components of the fluid exudate are also chemotactic, allowing them to home in to exactly where the injury occured. Once these cells are in contact they further amplify the chemoattractant mechanisms allowing more cells and fluid to be attracted to the area.  

#** The emigrated leukocytes and components of the fluid exudate are also chemotactic.

#** More cells and fluid are attracted to the area.  

# '''Emigration of red blood cells'''

# '''Emigration of red blood cells'''

#* [[Erythrocytes|Erythrocytes]] migrate through the gaps in the altered endothelium to the damaged tissue.

#* Once the gaps are big enough [[Erythrocytes|Erythrocytes]] can migrate through the gaps in the altered endothelium to the damaged tissue.

# '''Induction of an increase in temperature'''

# '''Induction of an increase in temperature'''

#* This may occur either locally or systemically.

#* This rise in temperature may occur either locally or systemically. A systemic rise in temperature is known as pyrexia. Occurs in general acute inflammation, and is often a sign of infection. To raise the body temperature, pyrogens are released which act on the temperature control centres in the hypothalamus, and are released from [[Macrophages|macrophages]] in particular, but also [[Neutrophils|Neutrophils]] and [[Eosinophils|eosinophils]]. Again, the [[Cytokines|cytokines]] TNF-α, Il-1 and IL-6 are all important in producing this pyrogenic response. These are termed '''endogenous pyrogens''' as they are endogenous to the body and not from an external source. Other pyrogens include the cellular coat of gram-negative organisms, the necrosis of damaged tissue cells, antigen-antibody complexes, and tumours (particularly those which have metastasised, though it may be difficult to separate this from the pyrexia caused by the central necrosis in such tumours).

#* A systemic rise in temperature is known as pyrexia.

#** Occurs in generalise acute inflammation.  

#** Pyrogens act on the temperature control centres in the hypothalamus, and are released from:

#*** [[Neutrophils|Neutrophils]], [[Eosinophils|eosinophils]] and [[Macrophages|macrophages]]

#**** Particulary [[Neutrophils|neutrophils]] when they begin to phagocytose.

#*** The cellular coat of gram-negative organisms.

#*** Necrosis of damaged tissue cells.

#*** Antigen-antibody complexes.

#**** Particularly those which have metastasised  

#**** It may be difficult to separate this from the pyrexia caused by the central necrosis in such tumours.

==Cells==

==Cells==

[[File:WBC Migration Graph.png|thumb|right|500px|Graph illustrating the cellular response to inflammation]]

[[File:WBC Migration Graph.png|thumb|right|500px|Graph illustrating the cellular response of inflammation]]

*    The classical cells of acute inflammation are   [[Neutrophils|neutrophils]], [[Eosinophils|eosinophils]],   [[Macrophages|macrophages]], [[Mast Cells|mast cells]] and    [[Basophils|basophils]] at an early stage of the inflammatory response, with the [[Lymphocytes|lymphocytes]] and [[Fibroblasts|fibroblasts]] forming the later stages.

*    The classical cells of acute inflammation are [[Neutrophils|neutrophils]], [[Eosinophils|eosinophils]], [[Macrophages|macrophages]], [[Mast Cells|mast cells]] and    [[Basophils|basophils]] at the acute phase of the inflammatory response, with the [[Lymphocytes|lymphocytes]] and [[Fibroblasts|fibroblasts]] forming the later, resolving stages.

** [[Macrophages|Macrophages]] are a common feature of acute and chronic inflammation.

<p> The [[Macrophages|Macrophages]] are a common feature of acute and chronic inflammation. </p>

[[Category:Acute Inflammation|A]]

[[Category:Acute Inflammation|A]]

[[Category:To Do - GenPath]]

[[Category:To Do - GenPath]]