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- 2. Normal Haemostasis Process of maintaining blood in a fluid, clot – free state in normal vasculature and rapidly forming a localized haemostatic plug at the site of vascular injury The pathologic opposite of haemostasis is thrombosis
- 4. Thrombosis Formation of solid mass in circulation from the constituents of flowing blood with intact cardiovascular tree during life
- 8. RUDOLF VIRCHOW Coined the terms “THROMBOSIS” and “EMBOLISM”
- 10. Endothelial Injury Main cause for thrombus formation in the heart and the arterial circulation These are platelet – rich clots Inflammation Infection Toxins from cigarette smoking Hypercholesterolemia
- 14. Abnormal blood flow Turbulence • Arterial thrombosis • Atherosclerotic plaque Stasis • Venous thrombosis • Aortic aneurysm • Post MI – cardiac mural thrombi • Rheumatic mitral valve stenosis • Hyperviscosity – Polycythemia vera
- 15. Hypercoagulability Thrombophilia Any disorder of blood that predisposes to thrombosis Hypercoagulable states are associated with VENOUS THROMBOSIS
- 16. Hypercoagulable states GENETIC Factor V mutation Increased levels of factor VIII, IX, XI or Fibrinogen ACQUIRED Prolonged bed rest or immobilization Disseminated Cancer Prosthetic cardiac valves Disseminated intravascular coagulation Oral contraceptive use Pregnancy and post partum
- 17. Arterial thrombi Venous thrombi Arteries and heart veins Aorta, coronary, cerebral etc Superficial varicose veins, deep leg veins Endothelial cell injury Causes-atherosclerosis, vasculitis, trauma Venous stasis Usually mural, not occluding lumen Invariably occlusive Grey- white, friable with lines of zahn Red-blue with fibrin strands with line of zahn Grows retrogrde Grows in the direction of blood flow Meshwork of platelets, fibrin, red cells and degenerating leucocytes More enmeshed RBC s and few platelets(red or stasis thrombi)
- 18. Antemortem thrombus Postmortem clot Adherent to wall Not adherent to vessel wall Red in colour Fibrin with red cells and leucocytes in a haphazard network (gelatinous) Upper layer resembling chicken fat Lines of zahn present No lines of zahn – bland and non – laminated
- 19. Lines of zahn
- 20. Mural thrombi
- 21. Vegetations – Thrombi on heart valves
- 23. Fate of thrombus Propagation Embolization – thrombi dislodges and travels to other sites in vasculature Dissolution – by fibrinolysis Organisation and recanalization Older thrombi become organised by ingrowth of endothelial cells, smooth muscle cells and fibroblasts. Capillary channels reestablish continuity of lumen
- 26. Embolism An embolus is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from origin.
- 27. Classification Thromboembolism (most common) Fat embolism Air embolism Amniotic fluid embolism
- 28. Pulmonary embolism Embolus lodges in the lungs (most common from deep vein thrombosis) Systemic embolism extremities, kidneys, Brain, lower intestines, spleen(arterial emboli from valvular intracardiac mural or thrombi, aortic aneurysms, atherosclerotic plaques)
- 29. Pulmonary thromboembolism Cause from venous emboli from deep leg veins Common in hospitalised and bed ridden patients Large thrombus gets impacted at bifurcation of pulmonary artery-saddle embolus Multiple emboli Paradoxical embolism
- 31. Fat embolism Obstruction of arterioles and capillaries by fat globules Fractures of long bones Trauma to soft tissue eg., adipose tissue Clinical features Pulmonary insufficiency - tachypnea, dyspnea, tachycardia Neurologic symptoms - irritability, restlessness to delirium and coma Thrombocytopenia
- 32. Fat embolism
- 33. Air embolism Gas bubbles within the circulation can coalesce to form frothy masses and obstruct vascular flow Large volume of air (more than 100 cc) is necessary to produce effect in pulmonary circulation Small volume of air trapped in coronary artery during bypass surgery Chest wall injury Obstetric or laproscopy procedures
- 34. Decompression sickness • Bends - formation of gas bubbles in skeletal muscles and joints producing pain - edema, focal • In lungs hemorrhages, atelectasis Caissons disease (chronic decompression sickness) - gas emboli in heads of femur, tibia and humeri.
- 35. Amniotic fluid embolism partum During labour or immediate post period Dyspnea, cyanosis, hypotensive shock, seizure and coma Infusion of amniotic fluid or fetal tissue into maternal circulation via tear in placental membranes or rupture of uterine veins
- 36. INFARCT Def: An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Aetiology Thrombosis or embolism Venous outflow obstruction (single outflow organs) Others : Hypotensive,local vasospasm, compression of, vessel by hematoma or tumor, torsion
- 37. Infarction Tissue necrosis due to ischaemia vascular insufficiency of any cause usually arterial occlusion due to thrombosis/embolism Mainly due to oxygen deficiency, but toxin accumulation & reperfusion injury may contribute Number of determining factors Size of vessel and size of vascular territory Partial / total vascular occlusion Duration of ischaemia
- 38. Infarct Development Dependent on a number of factors Nature of vascular supply Dual supply e.g. lungs, liver End arteries e.g. kidneys, spleen Rate of vascular occlusion Time for development of collateral circulation Vulnerability to hypoxia Neurons – 2-3mins, Myocardium – 20-30mins, Fibroblasts – hours. Oxygen content of blood Anaemia, cyanosis, congestive heart failure Can result in infarction due to otherwise inconsequential blockage Size of vessel and size of vascular territory Partial / total vascular occlusion Duration of ischaemia
- 39. Morphological Classification of infarcts Colour-Pale/anemic/white Red (hemorrhagic) Infarct Septic or bland
- 40. Appearance of Infarct ARTERY OCCLUSION NORMAL TISSUE INFARCTED TISSUE SURFACE FIBRINOUS EXUDATE ILL-DEFINED INFARC2nTdYear Pathology 2010 BORDERS
- 41. Types of Infarct Red (haemorrhagic) infarcts 1. 2. 3. 4. 5. Venous occlusion/congestion e.g. torsion Loose tissues where haemorrhage can occur and blood can collect in infarcted zone e.g. lung Tissues with dual blood supply e.g. lung small intestine (permitting blood flow from unobstructed vessel into infarcted zone – note flow is insufficient to rescue ischaemia) Tissues that were previously congested due to sluggish venous outflow When flow is re-established e.g. fragmentation of an occlusive embolus, angioplasty White infarcts 1. 2. arterial occlusion solid tissues, where haemorrhage limited e.g. spleen, heart, kidney
- 42. Pale / White Infarct Ischemia following obstruction of nutrient artery or hypoperfusion of tissue Solid organs with end-arterial circulation such as kidney, heart, spleen Wedge shaped.occluded vessel at the apex,base at the serosal surface Better defined with time, paler, hyperemic margins
- 43. 2nd Year Pathology 2010 Types of Infarct White splenic infarct
- 44. Microscopy Ischemic coagulative necrosis Demonstrable only >12-18 hrs. Inflammation in response to necrosis Phagocytosis of cellular debris by neutrophils & macrophages 1-2 days Healing response Scar tissue (brain- liquefactive necrosis)
- 45. Red (hemorrhagic)infarcts Sites :venous occlusion of organ with single venous outflow e.g. testicular torsion Loose tissues- e.g. lung Tissues with dual circulations: lung and gut Previously congested tissue With reperfusion of previously infarcted tissue
- 46. Types of Infarct Red pulmonary infarcts - dual pulmonary / bronchial2andrtYeerairaPla st h uo pl o pg y ly2 0 1 0
- 47. Pulmonary infarcts Ischemic necrosis of lung parenchyma following pulmonary embolism & lack of blood from bronchial arteries. When blood from bronchial arteries reperfuses the ischemic area, blood leaks into the alveolar spaces Appears triangular, red & airless. Becomes more firm &brown with time.
- 48. Septic infarct Following fragmentation of a bacterial vegetation from a heart valve or following microbes seeding a necrotic area. Converted into an abscess Greater inflammatory response scarring
- 49. Event Sequence 1. Coagulative necrosis 2. Infiltration by neutrophils 3. Infiltration by macrophages 4. Phagocytosis of debris 5. Granulation tissue formation 6. Scar formation
- 50. 2nd Year Pathology 2010 Time Microscopic Features Gross Features 0 – 4 hr None None 4 – 12 hr Early coagulation necrosis (nucleus: pyknosis, cytoplasm: eosinophilia) None 12 – 24 hr Further necrosis, haemorrhage, early neutrophil infiltrate Dark mottling 1 – 3 days Marked neutrophil infiltrate and necrosis Mottled with yellow-tan necrotic centre 3 – 7 days Early phagocytosis of dead cells by macrophages (at border) Hyperaemic border, central yellow-tan softening 7 – 10 days Well-developed phagocytosis, early granulation tissue formation Maximal yellow-tan softening, depressed red-tan margins 10 – 14 days Well-developed granulation tissue, early collagen deposition Red-gray depressed infarct borders 2 – 8 wk Increased collagen deposition, decreased cellularity Grey-white scar progresses from border toward centre > 2 months Acellular collagenous scar Dense gray scar