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Infarction

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pathology

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Infarction

  1. 1. GOOD MORNING DR V.VASUNDHARA DEPARTMENT OF CONSERVATIVE DENISTRY AND ENDODONTICS.
  2. 2. INFARCTION 2
  3. 3. CONTENTS Definition Etiology Types Pathogenesis Pathologic changes Infarcts of different organs References
  4. 4. DEFINITION Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage………………….ROBBINS
  5. 5. ETIOLOGY •Most Commonly,Infarcts are caused by Interruption in arterial blood supply, called ischemic necrosis •Less commonly,Venous obstruction can produce infarcts termed stagnant hypoxia
  6. 6. •Generally,Sudden, complete and continuous occlusion by thrombosis or embolism •Torsion of a vessel, e.g. in testicular torsion •Traumatic rupture or vascular compromise by edema, e.g. anterior compartment syndrome. • Nonocclusive circulatory insufficiency.
  7. 7. TYPES COLOUR Red or hemorrhagicPale or anemic
  8. 8. • Depending on Age a.Recent or fresh. b.Old or healed. •Presence or absence of infection. a.Bland – when free of bacterial contamination b.Septic – when infected.
  9. 9. PATHOGENESIS Localized hyperemia Edema and hemorrhage Cellular changes Progressive proteolysis of necrotic tissue and lysis of red cells An acute inflammatory reaction and hyperaemia Blood pigments liberated by hemolysis Progressive ingrowth of granulation tissue
  10. 10. PATHOLOGIC CHANGES •Grossly, infarcts of solid organs -wedge-shaped • apex -pointing towards occluded artery wide base - on the surface of the organ. •Infarcts due to arterial occlusion -pale venous obstruction - hemorrhagic. •Most infarcts become pale later as the red cell are lysed but pulmonary infarcts never become pale due to extensive amount of blood.
  11. 11. •Cerebral infarcts : poorly defined with central softening (encephalomalacia). •Recent infarcts : slightly elevated over the surface • Old infarcts : shrunken , depressed under the surface of the organ.
  12. 12. Microscopically •The pathognomic cytologic change in all infarcts is coagulative (ischaemic) necrosis of the affected area of tissue or organ. •In cerebral infarcts- characteristic liquefactive necrosis.
  13. 13. At periphery of an infarct, inflammatory reaction is noted. Initially neutrophils predominate ,later macrophages and fibroblasts appear. Eventually, necrotic area is replaced by fibrous scar tissue, may show dystrophic calcification. In cerebral infarcts, the liquefactive necrosis is followed by gliosis i.e. replacement by microglial cells distended by fatty material (gitter cells).
  14. 14. INFARCTS OF DIFFERENT ORGANS Location Gross appearance Outcome 1 Myocardial infraction Pale Frequently lethal 2 Pulmonary infraction Hemorrhagic Less commonly fatal 3 Cerebral infraction Hemorrhagic & Pale Fatal if massive 4 Intestinal infraction Hemorrhagic Frequently lethal 5 Renal infraction Pale Not lethal unless massive & bilateral 6 Infract spleen Pale Not lethal 7 Infract liver Pale Not lethal 8 Infracts of lower extremity Pale Not lethal
  15. 15. LUNG INFARCTION •Embolism of the pulmonary arteries • May occur in patients who have inadequate circulation : Chronic lung diseases • Congestive heart failure.
  16. 16. GROSS: pulmonary infarcts : wedge-shaped Base on the pleura, hemorrhagic, variable in size lower lobes. Cut surface : dark purple Shows blocked vessel near the apex of the infarcted area. Old organized and healed pulmonary infarcts appear as retracted fibrous scars.
  17. 17. Microscopically • Characteristic histologic feature : coagulative necrosis of the alveolar walls. •Initially: infiltration by neutrophils and intense alveolar capillary congestion hemosiderin, phagocytes and granulation tissue.
  18. 18. KIDNEY INFARCTION Renal infarcts are Common caused by Thromboemboli most commonly originating from heart such as mural thrombi in the left atrium ,MI,Vegetative endocarditis Less commonly renal artery atherosclerosis, arteritis sickle cell anemia.
  19. 19. Grossly:multiple and bilateral Characteristically:wedge shape Base - under capsule Apex-pointing towards medulla Narrow rim of preserved renal tissue is spared Cut surface in first 2 to 3 days : red and congested 4th day: centre turns pale yellow. 1 week: typically anemic , depressed below the surface
  20. 20. Microscopically Characteristic: affected area shows coagulative necrosis of renal parenchyma i.e. ghosts of renal tubules and glomeruli without intact nuclei and cytoplasmic content. The margin of the infarct shows inflammatory reaction – initially acute but later macrophages and fibrous tissue predominate.
  21. 21. INFARCT SPLEEN •Common site for infarcts •It results from Occlusion of one of the splenic arteries or its branches. Most common cause : thromboemboli arising in heart (eg.mural thrombi in the left atrium vegetative endocarditis myocarditis myocardial infarction)
  22. 22. •Less frequently by obstruction of microcirculation (e.g. in myeloproliferative diseases, sickle cell anemia, arteritis, Hodgkin's disease, bacterial infections). •Grossly, splenic infarcts are often multiple. •Characteristically pale or anemic, wedge-shaped • base - at the periphery • apex -pointing towards hilum.
  23. 23. •Features are similar to those found in anemic infarcts in kidney. •Coagulative necrosis and inflammatory reaction are seen. •Later, the necrotic tissues is replaced by shrunken fibrous scar. MICROSCOPICALLY
  24. 24. INFARCT LIVER • Uncommon • Dual blood supply •Obstruction of the portal vein is usually secondary to other diseases : Hepatic cirrhosis, IV invasion of primary CA of liver, CA of pancreas • Generally does not produce ischemic infarction but instead reduced blood supply to hepatic parenchyma causes non-ischemic infarct called infarct of Zahn.
  25. 25. •Obstruction of the hepatic artery or its branches: arteritis, arterio-sclerosis, bland or septic emboli. •Grossly, anemic but sometimes hemorrhagic due to stuffing of the site by blood from the portal vein. •Infarcts of Zahn (non-ischemic infarcts) produce sharply defined red-blue area in liver parenchyma.
  26. 26. Microscopically Infarcts of Zahn occurring due to reduced portal blood flow result in atrophy of hepatocytes and dilatation of sinusoids .
  27. 27. CEREBRAL INFARCTION •Local vascular occlusion •Occasionally, non-occlusive cause compression of the cerebral arteries from outside and from hypoxic encephalopathy.
  28. 28. •Clinically, the signs and symptoms depend upon the region infarcted. •In general, the focal neurologic deficit termed stroke, is present. •However, significant atherosclerotic cerebrovascular disease may produce transient ischemic attacks (TIA).
  29. 29. ARTERIAL OCCLUSION •Occlusion of the cerebral arteries by thrombi- common •Embolic arterial occlusion is commonly derived from the heart mural thrombosis complicating MI arterial fibrillation and endocarditis.
  30. 30. VENOUS OCCLUSION • Infrequent phenomenon due to good communications of the cerebral venous drainage. •However in cancer, due to increased predisposition to thrombosis, superior sagittal thrombosis may occur leading to bilateral, parasagittal, multiple hemorrhagic infarcts.
  31. 31. NON-OCCLUSIVE CAUSES Compression of the cerebral arteries from outside occurs during herniation
  32. 32. PATHOLOGIC CHANGES • Anemic or hemorrhagic • Affected area : soft and swollen blurring of junction between grey and white matter.
  33. 33. •Within 2-3days, the infarct undergoes softening and degeneration. • Central liquefaction with peripheral firm glial reaction • thickened leptomeninges, forming a cystic infarct. • Hemorrhagic infarct : red and superficially resembles a hematoma
  34. 34. MYOCARDIAL INFARCTION  Most Important consequence of coronary artery disease  Patient may die within first few hours of the onset while remainder suffer from effects of cardiac function  INCIDENCE:Occurs at all age but more common in elderly.
  35. 35. PREDISPOSING FACTORS FOR CORONARY ARTHEROSCLEROSIS  Hyperlipidaemia  Hypertension  DM  Cigarette smoking etc  DOCUMENTED WELL BY AUTOPSY STUDIES AND CORONARY ANGIOGRAPHIC STUDIES.
  36. 36. ETIOPATHOGENESIS 1.Mechanism of myocardial ischemia 2.Role of platelets 3.Complicated plaques 4.Non – atherosclerotic causes 5.Transmural versus subendocardial infarcts
  37. 37. MECHANISM OF MYOCARDIAL ISCHEMIA DIMINISHED CORONARY BLOOD FLOW Coronary artery disease,shock •MYOCARDIAL OXYGEN DEMAND •Exercise,emotion HYPERTROPHY OF HEART W/O SIMULTANEOUS INCREASE IN CORONARY BLOOD FLOW Hypertension,Valvular heart disease
  38. 38. ROLE OF PLATELETS •Rupture of atherosclerotic plaque exposes : sub endothelial collagen to platelets which undergo aggregation, activation & release reaction. •These events contribute to the build up of the platelet mass that gives rise to emboli or initiate thrombosis.
  39. 39. COMPLICATED PLAQUES Two complications occur Superimposed coronary thrombosis – seen in about half of the cases of acute MI. Infusion of fibrinolysins in the first few hours of development of acute MI in such cases restores blood flow in the blocked vessel in majority of cases. Intramural hemorrhage – is found in about one third of cases of acute MI. Hemorrhage and thrombosis may occur together in some cases.
  40. 40. NON-ATHEROSCLEROTIC CAUSES Coronary vasospasm Coronary ostial stenosis, Embolism, Thrombotic diseases, Trauma and outside compression.
  41. 41. 1 Feature Transmural infract Subendoc ardial infarct 1 Definition Full-thickness, solid Inner third to half, patchy 2 Frequency Most frequent (95%) Less frequent 3 Distribution Specific area of coronary supply Circumferent ial 4 Pathogenesis > 75% coronary stenosis Hypoperfusio n of myocardium 5 Coronary thrombosis Common Rare 6 Epicarditis Common None
  42. 42. LOCATION OF INFARCTS • LV •RV is less susceptible , due to its thin wall, having less metabolic requirements and is thus adequately nourished •Atrial infarcts, whenever usually accompany infarct of LV •LA is relatively protected because it is supplied by oxygenated blood in the left atrial chamber.
  43. 43. REGION OF INFARCTION Area of obstructed blood supply by one or more of three coronary arterial trunks in descending order: 1.Left anterior descending coronary artery :40 to 50% 2.Right coronary artery :30 to 40% 3.Left circumflex coronary artery:15 to 20%
  44. 44.  3 Regions of myocardial infraction. Stenosis of the left anterior descending coronary artery is the most common (40- 50%).  Region of infarction in the anterior part of the left ventricle including the apex and the anterior two-thirds of the interventricular septum.
  45. 45. Stenosis of the right coronary artery is the next most frequent (30-40%) .  It involves the posterior part of the left ventricle and the posterior one- third of the interventricular septum.
  46. 46. Stenosis of the left circumflex coronary artery is seen least frequently (15-20%).  Its area of involvement is the lateral wall of the left ventricle.
  47. 47. 50 Microscopically The changes are similar in both transmural and subendocardial infracts. There is ischemic coagulative necrosis of the myocardium which eventually heals by fibrosis. However, sequential microscopic changes are observed.
  48. 48. REFERENCES 1.Robbins and Cotran - Pathologic basis of diseases. 8th edition. 2. Harsh Mohan – Text book of pathology. 3rd edition. 3.Mc Gee, Isaacson and Wright – Oxford text book of Pathology. Principles of Pathology volume 1. 4.Anderson’s Pathology – 10th edition
  49. 49. God gave us healing hands ..……. To heal the wounds of the world

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