Infarction pathology lecture medical.pptx

Infaction

1. Infarction BY Dr. Faiqa Shahid

2. Infarction An infarct is an area of ischemic necrosis caused by occlusion of vascular supply to the affected tissue Infarction of heart and brain is a common cause of clinical illness Myocardial or cerebral infarctions are cause of cardiovascular diseases (40% deaths) Ischemic necrosis of distal extremities (gangrene) occurs in diabetic patients

3. Causes of infarction Arterial thrombi or arterial emboli (99%) Local vasospasm Expansion of atheroma secondary to intraplaque hemorrhage Extrinsic compression of vessel by tumor Vessel twisting Traumatic rupture of artery

4. Types of infarcts Red or h emorrhagic infarcts; Venous occlusion e.g. ovarian torsion Loose spongy organs e.g. lungs Tissues with dual circulation e.g. lungs or small intestine Previously congested tissues (due to sluggish venous outflow) Flow is reestablished after infarction e.g. after angioplasty White or anemic infarcts; Arterial occlusion Solid compact organs Organs with end arterial supply e.g. kidney, spleen

5. Septic infarcts; Occur with embolization of cardiac valve vegetation or when microbes seed necrotic tissues Infarct is converted into an abscess with a corresponding greater inflammatory response and healing by organization and fibrosis

6. Morphology of infarct Wedge shaped Apex is formed by occluded vessel and base is formed by periphery Margins are irregular or not well-defined which affect the vascularity of tissue from adjacent vessels Acute or fresh infarcts are poorly defined and hemorrhagic With time edges become better defined by a narrow rim of hyperemia due to inflammation White infarcts are progressively paler and more sharply defined with time due to limited amount of hemorrhage

7. Red infarcts have extensive hemorrhage and later on they become brownish because extravasated red cell are phagocytosed by macrophages and hemoglobin is converted into hemosiderin, brown residue Histological examination shows ischemic coagulative necrosis in which tissue architecture is preserved but nuclear details are lost Inflammatory response begins to develop along the margins of infarct within a few hours and well defined within 1-2 days followed by repair Most infarcts are replaced by a scar except brain in which ischemic tissue injury results in liquefactive necrosis

8. Factors that influence infarct development Anatomy of the vascular supply; The presence or absence of an alternative blood supply is the imp factor to determine whether occlusion of individual vessel causes damage. E.g. dual blood supply of lungs by pulmonary and bronchial arteries means that obstruction of pulmonary artery does not cause infarction unless bronchial circulation is also compromised. Similarly, liver which receives its blood supply from hepatic artery and portal vein, and hands and forearms with parallel radial and ulnar arterial supply are resistant to infarction. By contrast kidney and spleen both have end-arterial circulation and arterial obstruction causes infarction in these tissues.

9. Rate of occlusion; Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral circulation. E.g. interarteriolar anastomoses, which normally carry minimal blood flow, interconnect three major coronary arteries. If one coronary artery is slowly occluded, blood flow in this collateral circulation prevents infarction even if the original artery is completely occluded.

10. Tissue vulnerability to hypoxia; Neurons undergo irreversible damage when deprived of their blood supply for only 3-4 mint. Myocardial cells die after 20-30 mint of ischemia. By contrast, fibroblast within myocardium remain viable after many hours of ischemia.