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Infarction: Types and Pathogenesis

The document defines infarction and discusses its causes, types based on color, pathogenesis, vulnerability of tissues to hypoxia, pathologic changes microscopically, and healing process. Infarction is caused by occlusion of arterial supply or venous drainage and is a major cause of death. Types include pale and red infarcts depending on arterial or venous occlusion. Pathogenesis involves local anoxia and cell death over time. Tissue vulnerability to hypoxia determines likelihood of infarction. Pathologic changes include wedge-shaped lesions and coagulative necrosis replaced by scarring over time.

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19 views2 pages

Infarction: Types and Pathogenesis

The document defines infarction and discusses its causes, types based on color, pathogenesis, vulnerability of tissues to hypoxia, pathologic changes microscopically, and healing process. Infarction is caused by occlusion of arterial supply or venous drainage and is a major cause of death. Types include pale and red infarcts depending on arterial or venous occlusion. Pathogenesis involves local anoxia and cell death over time. Tissue vulnerability to hypoxia determines likelihood of infarction. Pathologic changes include wedge-shaped lesions and coagulative necrosis replaced by scarring over time.

Uploaded by

noreentamer20
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

INFARCTION

INFARCTION
Definition :
area of ischemic necrosis caused by 40% of all deaths in the
occlusion of the arterial supply or United States are caused
the venous drainage by cardiovascular disease,

Causes of infarction :
1-Thrombi and emboli ( most common )
2-Local spasm of the artery or torsion of vessels
3-Extrinsic compression of vessel by tumor
4-Rupture of the artery
Types of infarction
- -

COLOUR Presence or absence of infection

Pale Red: Septic:


Occur : in solid organs - Occur: in double circulation Aseptic: when there is
Due to : arterial occlusion - Due to : venous occlusion. free of infarction infection
Example : heart spleen ,kidney - Example: Lung & small intestine
-11
PATHOGENESIS : Rate of development of occlusion:
❖ Local anoxemic occurs after obstruction of the blood supply. ❖ Slowly developing occlusions are less to cause infarction
❖ Within few hours the affected part becomes swollen due to edema
and hemorrhage. Because it provide time for development pathways of flow
❖ being more marked in the lungs , and less extensive in the kidneys (collateral circulation)
and heart. ❖ Example: Coronary arteries
❖ Cellular changes such as swelling and degeneration appears early,
❖ death of the cells or necrosis occurs in 12-48 hours
085
❖ The availability of blood supply is the most factor determining
occlusion of a vessel will cause damage.
Vulnerability of hypoxia :
DEF : The susceptibility of a tissue to hypoxia influenced the
❖ Examples: Lung , Liver likelihood of infarction
❖ Both have dual circulation Examples:
❖ Therefor obstruction of small arteriole does not cause infarction 1) Neurons irreversible damage
2) Myocardial cell die after only 20-30 min
3) Skeletal muscles can survive longer time
Pathologic Changes:
❖ infarcts of solid organs :
1) wedge-shaped apex
2) pointing towards occluded artery wide base
3) on the surface of the organ.

❖ Most infarcts become :


1) pale because the red cell are lysed
2) pulmonary infarcts never become pale due to extensive amount of blood.

❖ Infarcts due to :
1) Arterial occlusion
2) pale
3) Venous obstruction
3) hemorrhagic.

Microscopically :
❖ The pathognomic change in all infarcts is coagulative (ischaemic) necrosis of the affected
area of tissue or organ.

❖ In cerebral infarcts:
characteristic liquefactive necrosis.

inflammatory reaction is noted.


first

Initially neutrophils predominate ,later macrophages and fibroblasts


-

appear.
Finally
Eventually, necrotic area is replaced by fibrous scar.
-

In cerebral infarcts, the liquefactive necrosis is followed by gliosis.

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