Author, Donkey, Bureaucrats, Administrators
53,803
edits
Changes
Created page with "* The term "infarction" is used to describe the formation of a segmental or localised area of ischemic necrosis in a tissue or organ following occlusion of the blood supply in th..."
* The term "infarction" is used to describe the formation of a segmental or localised area of ischemic necrosis in a tissue or organ following occlusion of the blood supply in the absence of an adequate collateral circulation.
* In domestic animals, infarcts are most commonly the result of embolic arteriolar impaction.
** [[Embolism|Embolism]] can result from [[Thrombosis|thromboses]] in both arterial and venous systems.
* Infarctions may differ in nature.
** The may be:
*** Bland
*** Infected
**** Low virulence organisms.
*** Septic
**** Virulent organisms, often with toxins.
*** Neoplastic.
**** Neoplastic infarction is often the precursor to metastatic tumour growth.
===Appearance===
* Grossly, infacts appear as pale or red “wedges” .
** Shape can often be more irregular.
* Redness depends on:
** The relative blood content.
*** I.e. whether haemorrhage or adjacent venous engorgementis involved.
** Whether there is co-existing inflammation/ infection.
===Pathogenesis===
* The kidney is taken as an example of pathogenesis of an infarct.
** The events outlined below assume comeplete obstruction of a functional end-arteriole by a bland embolus.
# The first stage is occlusion of a functional end-arteriole, in this example at the cortico-medullary junction.
#* This results in wedge-shaped area of cortical ischemia within the first 12 hours.
# Following occlusion, there is stasis of blood, hypoxia, leakage from capillaries and venules, and dilatation of vascular anastomoses.
#* Blood becomes trapped in the affected area, leading to reddening of the wedge.
#* This is exacerbated by hypoxic degeneration of capillaries, plasma leakage and swelling.
#* Occurs 12-24 hours.
# The wedge undergoes [[Necrosis - Pathology#Coagulation Necrosis|coagulative necrosis]].
#* There is RBC haemolysis.
#* Cells at the periphery swell and break down to due upset in osmotic pressure.
#** There is also capillary congestion, haemorrhage and neutrophil infiltration at the periphery.
#* The squeezing effect tends to make the wedge become paler.
#* Occurs 24-36 hours.
# There is an inflammatory and demolition phase.
#* There is increased infiltration of polymorphs and macrophages in the peripheral zone.
#** The peripheral zone becomes more congested.
#* 36-72 hours.
# A healing phase follows.
#* Initially, macrophages and chronic inflammatory cells are present.
#* Later, there is granulation/ fibrous tissue replacement.
#* This phase may last up to 7-10 days or longer, depending on the nature of the lesion.
===Infarction in Specific Organs===
* Organs and tissues with good alternative blood supplies or less-dense parenchyma tend to accomodate congestion, haemolysis, oedema and inflammation better.
** For example, lung, [[Liver - Anatomy & Physiology|liver]], spleen and intestine.
** Infarcts tend to be red but are less wedge-shaped and softer than in the kidney.
** Infarcts in these organs are less common because of good collateral blood supplies.
* In the brain, infarction in cerebral arterioles leads to colliquative necrosis.
** Microglia are activated.
*** Some microglia phagocytose spilled myelin and become foamy Gitter cells.
[[Category:Circulatory Disorders - Pathology]]
* In domestic animals, infarcts are most commonly the result of embolic arteriolar impaction.
** [[Embolism|Embolism]] can result from [[Thrombosis|thromboses]] in both arterial and venous systems.
* Infarctions may differ in nature.
** The may be:
*** Bland
*** Infected
**** Low virulence organisms.
*** Septic
**** Virulent organisms, often with toxins.
*** Neoplastic.
**** Neoplastic infarction is often the precursor to metastatic tumour growth.
===Appearance===
* Grossly, infacts appear as pale or red “wedges” .
** Shape can often be more irregular.
* Redness depends on:
** The relative blood content.
*** I.e. whether haemorrhage or adjacent venous engorgementis involved.
** Whether there is co-existing inflammation/ infection.
===Pathogenesis===
* The kidney is taken as an example of pathogenesis of an infarct.
** The events outlined below assume comeplete obstruction of a functional end-arteriole by a bland embolus.
# The first stage is occlusion of a functional end-arteriole, in this example at the cortico-medullary junction.
#* This results in wedge-shaped area of cortical ischemia within the first 12 hours.
# Following occlusion, there is stasis of blood, hypoxia, leakage from capillaries and venules, and dilatation of vascular anastomoses.
#* Blood becomes trapped in the affected area, leading to reddening of the wedge.
#* This is exacerbated by hypoxic degeneration of capillaries, plasma leakage and swelling.
#* Occurs 12-24 hours.
# The wedge undergoes [[Necrosis - Pathology#Coagulation Necrosis|coagulative necrosis]].
#* There is RBC haemolysis.
#* Cells at the periphery swell and break down to due upset in osmotic pressure.
#** There is also capillary congestion, haemorrhage and neutrophil infiltration at the periphery.
#* The squeezing effect tends to make the wedge become paler.
#* Occurs 24-36 hours.
# There is an inflammatory and demolition phase.
#* There is increased infiltration of polymorphs and macrophages in the peripheral zone.
#** The peripheral zone becomes more congested.
#* 36-72 hours.
# A healing phase follows.
#* Initially, macrophages and chronic inflammatory cells are present.
#* Later, there is granulation/ fibrous tissue replacement.
#* This phase may last up to 7-10 days or longer, depending on the nature of the lesion.
===Infarction in Specific Organs===
* Organs and tissues with good alternative blood supplies or less-dense parenchyma tend to accomodate congestion, haemolysis, oedema and inflammation better.
** For example, lung, [[Liver - Anatomy & Physiology|liver]], spleen and intestine.
** Infarcts tend to be red but are less wedge-shaped and softer than in the kidney.
** Infarcts in these organs are less common because of good collateral blood supplies.
* In the brain, infarction in cerebral arterioles leads to colliquative necrosis.
** Microglia are activated.
*** Some microglia phagocytose spilled myelin and become foamy Gitter cells.
[[Category:Circulatory Disorders - Pathology]]