Infarction Yiran Ni M.D Department of pathology CTGU Mail: [email protected] Tel: 15997529140 Office...
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Transcript of Infarction Yiran Ni M.D Department of pathology CTGU Mail: [email protected] Tel: 15997529140 Office...
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InfarctionInfarction
Yiran Ni M.D
Department of pathology CTGU
Mail: [email protected]
Tel: 15997529140
Office room: S-2623
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Water
Blood
Trunk
Vessel
Leaves fall Tissue necrosis
Question 1
What is infarction?
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Definition
• An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.
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Common sites
• Infarction involving different organs is a common and extremely important cause of clinical illness.
• Myocardia infarction causes 17 million death world-wide annually(1million in China).
• Cerebral infarction causes 5 million death world-wide annually (1.5million in China).
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• Pulmonary infarction
• Bowel infarction
• Ischemic necrosis of the extremities (gangrene)
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Question 2:What are the common causes of infarction?
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Common causes
• Commonest cause:
• thrombotic or embolic events lead to arterial occlusion.
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• Expansion of an atheroma secondary to intraplaque hemorrhage
• Extrinsic compression of a vessel (e.g., by tumor).
• Local vasospasm
• Vessel twisting (e.g., in testicular torsion or bowel volvulus).
• Vascular compression by edema or entrapment in a hernia sac.
• Traumatic vessel rupture.
• venous obstruction(e.g., testis and ovary).
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Question 3:What are factors that influence
development of an infarct ?
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Factors that influence development of an infarct
• The major determinants include:
• (1) the nature of the vascular supply;
• (2) the rate of development of the occlusion; (3) the vulnerability of a given tissue to hypoxia;
• (4) the blood oxygen content.
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(1)The nature of the vascular supply
• The availability of an alternative blood supply is the most important factor in determining whether occlusion of a vessel will cause damage.
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Capillary Capillary networknetwork
bronchia
PAPA
BABA
PVPV
BVBV
The changes of the blood circulation when The changes of the blood circulation when embolism of pulmonary arteries occurembolism of pulmonary arteries occur
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(2)The rate of development of the occlusion
• Slowly developing occlusions are less likely to cause infarction because they provide time for the development of alternative perfusion pathways.
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(3)The vulnerability of a given tissue to hypoxia
• The susceptibility of a tissue to hypoxia influences the likelihood of infarction.
• Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes.
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(4)The blood oxygen content• The partial pressure of oxygen in blood also
determines the outcome of vascular occlusion. Partial flow obstruction of a small vessel in an anemic or cyanotic patient might lead to tissue infarction, whereas it would be without effect under conditions of normal oxygen tension. In this way, congestive heart failure, with compromised flow and ventilation, could cause infarction in the setting of an otherwise inconsequential blockage.
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Question 4:What are the typical morphologic
changes of an infarct ?
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Morphology of infarcts
(1) Shapes: depends on vascular distribution of
the organ
pyramid shaped infarct: kidney, lungs, and spleen
irregular, map shaped infarct: heart, brain
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pyramid shaped infarct:
kidney, lungs, and spleen
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Irregular, map shaped infarct: Irregular, map shaped infarct: heart, brainheart, brain
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(2)Texture: depends on pathological changes in
different organs
Coagulative necrosis – solid organs (kidenys,
spleen), lungs and intestine etc
Liquefactive necrosis – brain(cerebral malacia)-cyst
formation
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(3)Color of an infarct(3)Color of an infarct
• Infarcts are classified on the basis of their color (reflecting the amount of hemorrhage).
• Therefore, infarcts may be either red (hemorrhagic) or white (anemic) .
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Anemic infarcts (White infarcts)Anemic infarcts (White infarcts)
White (anemic) infarcts occur with arterial occlusions in
solid organs with end-arterial circulation (such as heart,
spleen, and kidney), where the solidity of the tissue limits
the amount of hemorrhage that can seep into the area of
ischemic necrosis from adjoining capillary beds .
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Morphology of anemic infarcts (White infarcts)
Organ involved: solid organs with deficient
collateral circulation of arteries (heart, kidneys,
spleen, etc.)
Grossly: wedge-like or triangular necrotic foci with
peripheral hemorrhagic zone
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Anemic infarcts of spleen
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Anemic infarcts of kidney
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Anemic infarcts of heart
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Microscopically:Microscopically: ischemic coagulative necrosis ischemic coagulative necrosis
The outline of tissue structure remains The outline of tissue structure remains
Nuclear changes: pyknosis, karyorrhesix, or Nuclear changes: pyknosis, karyorrhesix, or
karyolysis karyolysis
Leucocytic reaction at peripheral marginLeucocytic reaction at peripheral margin
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Anemic infarcts of heart muscle
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Anemic infarcts of kidneyAnemic infarcts of kidney
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Anemic infarcts of brain
Irregular shaped
Liquefactive necrosis
-cerebral malacia
-cyst formation
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Hemorrhagic infarcts (Red infarcts)Hemorrhagic infarcts (Red infarcts)Red (hemorrhagic) infarcts occur (1) with venous occlusions
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(2) in loose tissues (such as lung), which allow blood to collect in the infarcted zone
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(3) in tissues with dual circulations (e.g., lung and small intestine), permitting flow of blood from the unobstructed vessel into the necrotic zone (obviously such perfusion is not sufficient to rescue the ischemic tissues);
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(4) in tissues that were previously congested because of sluggish venous outflow;
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(5) when flow is re-established to a site of previous arterial occlusion and necrosis
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Question 5:The fate of an infarct
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Key points
• 1. Definiton
• 2. Causes
• 3. Determinants
• 4. Morphology
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