1. Chapter Three Hemodynamic Disorders

3. Hyperemia: Arterial hyperemia Venous hyperemia Section A

9. Pulmonary congestion Edema Hemorrhage Heart failure cells Brown induration

11. Acute pulmonary congestion

12. Chronic pulmonary congestion

14. Liver congestion Atrophy Fatty change Nutmeg liver Centrilobular necrosis liver cirrhosis

20. Cardiac cirrhosis of the liver in the longstanding cases

22. Thrombosis Thrombus Section B

24. Normal hemostatic process

30. Platelet adhesion and aggregation

32. Fibrinolytic system

37. Hypercoagulable states Primary (genetic): Antithrombin III deficiency Protein C deficiency Protein S deficiency Other combined deficiency

38. Hypercoagulable states Secondary (acquired): High risk: Prolonged bed rest or immobilization. Myocardial infarction. Tissue damage (surgery, fractures, burns). Cardiac failure. Cancer. Acute leukemia. DIC. Thrombotic thrombocytopenia.

39. Hypercoagulable states Secondary (acquired): Low risk: Atrial fibrillation. Cardiomyopathy. Nephrotic syndrome. Hyperlipidemia. Late pregnancy/postdelivery. Oral contraceptives. Lupus anticoagulant. Sickle cell anemia. Smoking. Thrombocytosis.

43. White thrombus Site: heart valve , artery Component: Platelet, fibrin

44. Mixed thrombus Site: heart chamber, vein Component: Platelet, fibrin,RBC

46. Mural thrombosis

47. Mural thrombosis

48. RED THROMBUS

52. Organization and recanalization of thrombus During organization, the thrombus dissolved and blood could flow again.

63. AMNIOTIC FLUID EMBOLISM Incidence: 1/50 000 deliveries Mortality rate: 80% Clinical onset: Sudden severe dyspnea, cyanosis, hypotensive shock, DIC

77. 3. Between the extremes of large and small emboli (10-15%): Pulmonary hemorrhage. 4. Multiple small emboli: Pulmonary hypertension and vascular sclerosis.

78. Systemic embolism I . 80-85% from heart, secondary to myocardial infarction. II . 5-10% from auricular thrombi associated with rheumatic heart disease and atrial fibrillation. III . 5% from the dilated cardiac chamber of myocarditis / cardiomyopathy. VI . Less common sources: Debris from ulcerative atheromata, or thrombi in aneurysms, infectious endocarditis, prosthetic valves, paradoxical emboli. V . Unknown.

81. Intrinsic occlusion for example, thrombosis, embolism expansion of atheroma Vasospasm Extrinsic compression for example, twisting of the vessels Etiology

94. Venous occlusions Loose tissues Tissues with dual circulations Tissues previously congested Blood flow reestablished Red infarct/hemorrhagic infarct

95. The alteration of blood in pulmonary embolism