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  1. ISCHEMIA AND INFARCTION Dr.V.Shanthi Associate Professor ,Department of Pathology Sri Venkateswara Institute of Medical Sciences Tirupathi.
  3. CONGESTION Heart failure left sided Back Pressure in pulmonary vessels CVC Lung Right sided Back pressure Systemic • CVC liver • CVC spleen • CVC kidney • CVC leg veins
  4. CVC LUNG Pathogenesis • Inability of the blood to return to left side of heart leading to stagnation of blood in lungs • Alveolar septa shows edema with dilated and congested capillaries • Rupture of these capillaries lead to intra alveolar hemorrhages • Breakdown of erythrocytes leads to release of hemoglobin which is ingested by macrophages called heart failure cells
  5. CVC LUNG Morphology Lungs – Heavy, Bulky and dark brown C/S frothy fluid, Solid with blood Late – firm and hard – fibrous – septa Cut section is rusty brown (iron deposition) – referred to as “brown induration”
  6. CVC LUNG Microscopic picture – Alveolar septa shows edema and fibrosis Alveolar spaces are filled with blood cells Hemosiderin pigment laden Macrophages in alveolar spaces - “ Heart failure cells”
  7. CVC – LIVER • Occurs in • right sided C.C.F • Hepatic vein obstruction • Occlusion of interior vena cava • Clinical – Tender liver Slight enlargement
  8. CVC – LIVER • Morphology – liver enlarged with tensed capsule • C/S – “Nut meg” liver Red & yellow, mottled appearance - Congested centre lobule - Fatty peripheral zone
  9. CVC – LIVER
  10. CVC – LIVER Acute hepatic congestion • Central vein and sinusoids are distended • Centrilobular area is at the distal end of the hepatic blood supply, hence centrilobular hepatocytes may undergo ischemic necrosis • Periportal hepatocytes are better oxygenated and undergo fatty change Chronic passive hepatic congestion • Centrilobular region undergo necrosis and appears red brown and depressed • This region is surrounded by pale areas of uncongested liver with fatty change
  11. CVC – LIVER Microscopically – centrilobular congestion and hemorrhage, hemosiderin laden macrophages and necrosis
  12. CVC SPLEEN • CVC Spleen occurs in - • Right side C.C.F • Portal hypertension • Cirrhosis of liver • Morphology- Early stages – slight to moderate enlargement Chronic – Progressive enlargement upto 1000gms (Normal – 150gms) Grossly spleen is deeply congested, tense and cyanotic Cut section – firm to gray tan – Congestive spleenomegaly
  13. CVC SPLEEN Microscopy • Capsule – thickened • Congestion & dilation of sinusoids • Recent & old hemorrhages with organization of hemorrhages • Gumma gandy bodies Sidero-fibrotic nodules with deposition of hemosiderin pigment and calcium salts • hyperplasia of red pulp • Common cause of hyper splenism
  15. ISCHEMIA & INFARCTION • Inadequate blood supply to a part of the body – ischemia • If ischemia persists beyond permissible limits – infarction Affects of ischemia causing deprivation of blood supply are - Deprivation of oxygen - Deprivation of nutrition - Failure to remove metabolic waste which accumulate and cause damage • Immediate effect of ischemia will be there on tissue with highest O2 requirements and metabolic demands- Brain and Heart
  16. ISCHEMIA & INFARCTION Causes of Ischemia • Generalized – hypovolemic shock (Cardiac failure) • Localized - Atherosclerosis Thrombosis Embolism Vasculitis Spasm of vessels External pressure
  17. ISCHEMIA & INFARCTION Localized causes – 3 levels – • Arterial • Venous • Microcirculation (arterioles, veinules, capillaries)
  18. ISCHEMIA & INFARCTION Causes of Arterial Obstruction Luminal occlusion (intraluminal) Causes in the arterial walls (intramural) Outside pressure on artery (extramural) • Thrombosis • Embolism • Vasospam • Arteriosclerosis • Polyarteritis nodosa • Thromboangitis obliterans • Hypothermia • Ergot poisoning • Torsion • Ligature • Torniquet
  19. ISCHEMIA & INFARCTION Causes of Venous obstruction Luminal occlusion Causes in vessel wall (intramural) Outside pressure on vein • Thrombosis • Embolism • Varicose veins of leg • Ligature • Hematoma • Strangulated hernia • Intussusception
  20. ISCHEMIA & INFARCTION Causes in microcirculation (arterioles, veinules and capillaries) Luminal occlusion Causes in microvascular wall (intramural) Outside pressure (extramural) Bedsores • Vasculitis – polyarteritis nodosa, Henoch schonlein purpura, arthus reaction • Frostbite injuring the wall of small vessels • By RBC’s – sickle cell anemia • By WBC’s – chronic myeloid leukemia • By precipitated cryoglobulins • Fat embolism • Air embolism
  21. ISCHEMIA & INFARCTION • Effect of ischemia:- 1.Functional disturbances:- eg: angina pectoris intermittent claudication manifested only by exertion 2. Degeneration, atrophy and replacement by fibrosis - gradual obstruction – adaptation 3. Gangrene – sudden or gradual complete obstruction 4. Infarction
  22. INFARCT • An area of ischemic necrosis caused by either occlusion of arterial blood or occlusion to venous drainage or both pathological process – infarction • Non ischemic necrosis is not infarct • Infarction differs from gangrene by absence putrefaction. Infarction is surrounded by living tissue • 99% of infarcts – arterial occlusion - thrombosis & embolism • Venous thrombosis – infarction – block in drainage - stagnant hypoxia
  23. Factors determining severity of ischemic injury Anatomic patterns General and cardiovascular status Type of tissue affected Rapidity of development Degree of vascular occlusion
  24. INFARCT • Anatomic patterns • Single arterial supply without anastomosis • Central artery of retina • Interlobular arteries of kidney • Single arterial supply with rich anastomosis • Superior mesenteric artery to small blood vessels • Inferior mesenteric artery to distal colon • Parallel arterial supply • Brain by circle of Willis • Forearm by radial and ulnar arteries • Double blood supply • Lungs – by bronchial circulation and pulmonary arterial branches • Liver – by portal circulation and hepatic arterial flow
  25. INFARCT General and cardiovascular status • Anemias • Lowered oxygenation of blood (hypoxaemia) • Marked coronary atherosclerosis • Cardiac failure • Blood loss shock
  26. INFARCT Type of tissue affected • Mesenchymal tissues are more resistant to ischemic affect than the parenchymal cells • Tissues sensitive to ischemia are • Brain (cerebral neurons) • Myocardial cells • Kidney ( especially epithelial cells of proximal convoluted tubules )
  27. INFARCT Rapidity of development – • sudden vascular obstruction causes severe ischemic damage • If develops gradually collaterals can develop and damage is less Degree of vascular occlusion – • complete vascular occlusion causes severe injury than partial obstruction
  28. INFARCT Pathogenesis Localized congestion immediately after obstruction of the blood supply Edema and hemorrhage Cellular changes Like cellular swelling, reversible changes and further irreversible changes Progressive proteolysis of necrotic tissue and lysis of RBC’s Acute inflammatory reaction and hyperemia Progressive in growth of granulation tissue
  29. INFARCT Types of infarct According to color According to age According to absence or presence of infection Pale or anemic Arterial occlusion in compact organs(kidneys, heart, spleen) Red or hemorrhagic In soft loose tissues, and in pulm arterial obstruction or by venous occlusion in intestines Recent or fresh Old or healed Bland – free of bacterial contamination Septic – when infected
  30. INFARCT Features Red infarct White infarct Cause • Venous occlusion • Arterial occlusion Types of tissues affected • Loose, spongy tissues eg lung where blood collects in infarcted zone • Dual blood circulation that allows blood to flow from an unobstructed parallel supply into necrotic zone • Tissues previously congested by venous outflow • When flow is reestablished to a site of previous arterial occlusion and necrosis (eg after angioplasty) • In solid organs • with end arterial supply where tissue density limits seepage of blood from adjoining capillary beds into necrotic area
  31. INFARCT Morphology • Wedge or pyramidal shape • Base towards periphery • Apex towards site of obstruction • Most often peripherally situated • Slow fibrinous exudate over serous coverings eg: Pleura
  32. INFARCT LUNG • Cause – Embolism of Pulmonary arteries • Lungs also receive blood supply from bronchial arteries • Infarction occurs when the person has inadequate circulation due to chronic lung disease and congestive cardiac failure
  33. INFARCT LUNG Grossly – • Shape - wedge shaped with base on the pleura • Size – variable • Site - most often in lower lobes • Fibrinous pleuritic covering lung • Cut surface – dark purple and may show the blocked vessel near the apex of infarcted area • Old organized and healed pulmonary infarcts appear as retracted fibrous scars
  35. INFARCT LUNG Microscopically - • Coagulative necrosis of the alveolar walls • Initially – infiltration by neutrophils and intense alveolar capillary congestion • Later their place is taken by hemosiderin, phagocytes and granulation tissue
  36. INFARCT KIDNEY Causes • Most common cause – thrombo emboli originating from the heart such as in mural thrombi in left atrium, myocardial infarction, vegetative endocarditis and from aortic aneurysms • Less commonly – renal artery atherosclerosis, arteritis and sickle cell anemia
  37. INFARCT KIDNEY Gross – • Often multiple and bilateral • Type of infarct – pale or white • Wedge shaped with base resting under the capsule and apex pointing towards medulla • Narrow rim of renal tissue under the capsule is spared as it draws its blood supply from the capsular vessels • Cut surface – in the 1st 2 to 3 days it is red and congested but by 4th day it becomes pale yellow • At the end of one week, infarct is typically anaemic and depressed below the surface of kidney
  38. INFARCT KIDNEY Microscopically • Affected area shows coagulative necrosis of renal parenchyma ( ghost tubules and glomeruli) • Margin of the infarct – inflammatory reaction – initially acute but later macrophages and fibrous tissue predominate
  40. INFARCT LIVER • Infarcts in the liver are uncommon due to dual blood supply from portal vein and hepatic artery • Obstruction of hepatic artery or its branches caused by arteritis, arteriosclerosis or bland/septic emboli – infarcts of liver • Obstruction of portal vein or its branches is usually secondary to diseases like cirrhosis, intravenous invasion of primary carcinoma of liver, carcinoma of pancreas and pyelophlebitis • This does not produce ischemic infarction but instead reduced blood supply to hepatic parenchyma causes non-ischemic infarct called – infarct of zahn
  41. INFARCT LIVER Grossly – • ischemic infarcts of the liver are usually anemic • But may be hemorrhagic due to stuffing of site by blood from portal veins • Infarcts of zahn produce sharply defined red-blue area in liver parenchyma
  42. INFARCT LIVER Microscopically • Infarcts of liver is characteristically pale and similar to that as in kidney or spleen • Infarcts of zahn occurring due to reduced portal blood flow over long duration result in chronic atrophy of hepatocytes and dilatation of sinusoids
  43. INFARCT SPLEEN • Results from occlusion of splenic artery or its branches • Occlusion is caused most commonly by • Thromboemboli arising in heart ( mural thrombi in left atrium, vegetative endocarditis, myocardial infarction) • Obstruction of microcirculation as in myeloproliferative diseases, sickle cell anemia, arteritis, Hodgkins disease, bacterial infection
  44. INFARCT SPLEEN Grossly • Often multiple • Characteristically pale or anemic and wedge shaped with base at the periphery and apex pointing towards hilum
  45. INFARCT SPLEEN Microscopically • Coagulative necrosis and inflammatory reaction is seen • Later necrotic tissue is replaced by shrunken fibrous scar
  46. PREVIOUS QUESTION PAPERS • CVC liver(Nutmeg liver)– causes, gross and microscopy (NTRUHS-Oct 2005, RGUHS- Jun 2010) • CVC Lung/Brown induration of Lung (RGUHS- Jun 2009, Jun 2010, Dec 2011,Jul 2012) • Chronic venous congestion – liver & lung (RGUHS- Dec 2012) • Define Infarction.Types of infarcts with examples and sites (RGUHS- Jun 2013, Dec 2013) • What are heart failure cells? Mention the special stain used for demonstration (RGUHS, July 2008) • Nutmeg liver • Define Infarction.Types of infarcts with examples and sites (RGUHS- Dec 2009, Jul 2012, Jun 2013)
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