|
Pulmonary Pathology Online Anatomy and Histology of the Normal Lung and Airways Examination of pulmonary and pleural biopsies Useful chromatic and immunostains in pulmonary pathology Percutaneous Needle and Trucut Biopsy Specimen Transbronchial Biopsy Specimen Transbronchial biopsy in lung transplant recipients Lobectomy and pneumonectomy specimen Histopathological reporting of pulmonary parenchymal biopsies Histopathological reporting of pulmonary biopsies in cases of Idiopathic Pulmonary Fibrosis Closed pleural biopsy for neoplasm or inflammatory lesions ; Open pleural biopsy and pneumonectomy or pleural stripping Anatomical Distribution of Pulmonary Disease Congenital Cystic Adenomatoid Malformation Bronchopulmonary Sequestration Acute Respiratory Distress Syndrome Neonatal Respiratory Distress Syndrome Complications of Neonatal Respiratory Distress Syndrome Pulmonary Eosinophilic Granuloma Pathological Diagnosis of Granulomatous Lung Diseases Infectious Granuloma of the Lung Non-necrotising Granulomatous Inflammation of the lung An approach to Histopathological Examination of Pulmonary Granulomatous Inflammation |
|
Infarction: Infarct is an area of ischemic necrosis due to occlusion of arterial supply in most cases. Diagram showing common sites of Systemic Infarction from Arterial Emboli: click here The word "infarction" comes from the Latin "infarcire" meaning "to plug up or cram." - Total occlusion of an artery produces an area of coagulative necrosis called an infarct. - Partial occlusion - that is, stenosis - occasionally causes necrosis, but more commonly leads to a variety of degenerative cell changes. These changes include vacuolization of cells, atrophy, loss of muscle cell myofibrils, and interstitial fibrosis. Infarction of vital organs such as the heart, brain, and intestine may be life-threatening. If the individual survives, the infarct heals with a scar, which is the common occurrence in less vital organs. Most cases of infarction are due to thrombosis or embolism. Rarely, there are other causes - Examples: vasospasm, extrinsic compression of a vessel by tumour, edema, or entrapment in a hernia sac, and twisting of vessels, such as testicular torsion or bowel volvulus. Traumatic vessel rupture is a very rare cause. Occluded venous drainage (e.g. venous thrombosis) can cause infarction but more often induce congestion only (due to rapid blood flow through collaterals).Infarcts due to venous thrombosis are more likely in organs with single venous outflow, such as testis or ovary. Pulmonary Infarction ; Myocardial Infarction Factors that influence development of an infarct: 1. Pattern of vascular supply: Organs with dual circulation (lung, liver) or anastomosing circulation (radial and ulnar arteries, circle of Willis, small intestine) protect against infarction. Organs supplied with end arteries (spleen, kidneys) usually develop infarct after occlusion of the arterial supply. 2. Rate of development of occlusion: Slowly developing occlusions less often cause infarction by providing time to develop alternate perfusion pathways. (Example: collateral coronary circulation). 3. Changes due to hypoxia: Neurons undergo irreversible damage after 3 to 4 minutes of ischemia, myocardial cells die only after 20 to 30 minutes. In contrast, fibroblasts within ischemic myocardium are viable even after many hours. 4. Oxygen content of blood: Anemia, cyanosis, or congestive heart failure (with hypoxia) may cause infarction. Infarct morphology: Morphologically, the necrotic tissue of an infarct swells, and the infracted area often protrudes above the surface of the organ. As an infarct ages it undergoes fibrosis, reduces in size, and ultimately shrinks below the surface of the organ. A fresh infarct is pale because of the loss of red blood cells, an appearance reflected in the terms “white” or “pale” infarct. Infarcts can also be red (hemorrhagic), particularly in the lung and the intestine. With time, the tissue surrounding an infarct forms granulation tissue rich in sprouting capillaries that bleed easily. Therefore, the border of a healing infarct frequently is hemorrhagic. Infarcts may also be either septic or bland Red infarcts occur: - In venous occlusion ( Example: ovarian torsion) - In loose tissues (such as lungs, placenta) - In tissues with dual circulation (Example: lungs and small intestine) - In tissues previously congested because of sluggish venous outflow. - At a site of previous occlusion and necrosis when flow is re-established. White infarcts occur in solid organs - Examples: heart, spleen and kidney, with end arterial circulation. Pathogenesis and pathology: Arterial obstruction causes fall of distal blood pressure to capillary pressure with dilation of capillaries causing injury due to anoxia. This is the commonest cause. Blood from the veins accumulates in the dilated and injured capillaries with outpouring of fluid and RBC into the surrounding tissue. Thus, the area becomes red, engorged and even hemorrhagic with venous blood, hence the term infarction. Gross features: -All infarcts tend to be wedge-shaped, the occluded vessel marks the apex, and the organ periphery forms the base. -Lateral margins may be irregular reflecting the pattern of adjacent vascular supply. Microscopic features: - Features of ischemic coagulative necrosis. - An initial inflammatory response. This may last for hours to days. - This is followed by a reparative response. This may last from days to weeks. - The changes usually begin in the preserved margin. - In stable or labile tissues, some parenchymal regeneration may occur where the underlying stromal architecture is spared. - Most infarcts are ultimately replaced by scar tissue. The brain is an exception. In the brain there is liquifaction followed by absorption and cyst formation. - Septic infarctions occur with embolization of infected cardiac vegetations or when microbes seed an area of necrosis. - The infarct becomes an abscess. - Abscess slowly organize to scar.
Custom Search
|
|
1.
Location : Myocardial infarction Gross appearance: Pale Lethality: Frequently lethal 2. Location : Pulmonary infarction Gross appearance: Hemorrhagic Lethality: Less commonly fatal 3. Location : Cerebral infarction Gross appearance: Hemorrhagic or pale Lethality: Lethal only of massive 4. Location : Intestinal infarction Gross appearance: Hemorrhagic Lethality: Frequently lethal 5. Location : Renal infarction Gross appearance: Pale Lethality: Not lethal unless massive and bilateral |
FUNCTIONAL ANATOMY OF THE HEARTANATOMY OF THE CORONARY ARTERIES AUTOPSY EXAM. OF CORONARY ARTERIES MITRAL, PULMONARY AND TRICUSPID VALVE LESIONS Myocardial infarctionhypertensive heart diseasepericardial disease |