1. HEMODYNAMIC DISORDERS, THROMBOSIS AND SHOCK

2. Edema

3. Fluid Balance Across Capillary Walls Factors Involved
Interstitial Fluid
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.

4. Edema - Pathogenesis

5. Edema

7. Edema: Lymphatic Obstruction

10. Pulmonary Edema
This is the alveolar spaces filled with extravasated fluid from the congested blood vessels. This is typically seen in the setting of left ventricular failure where blood is not efficiently pumped out of the heart and therefore is gets backed up in the lungs. The lungs fill with this fluid and will be 2-3 times their weight.

11. Fluid in Trachea/Bronchi
When this becomes overwhelming for the small alveolar spaces we see fluid coalesce into froth in the airways. The froth is a mixture of air, edema fluid and sometimes can have extravasated rbcs so the froth can sometimes be pink.

12. Abdominal Ascites
Again we see large amounts of accumulated fluid into the abdomen and we can see these large engorged blood vessels that have an enormous amount of hydrostatic pressure in the abdomen. Called caput medusa as most of these patients have blood vessels coalescing around the navel giving it a snake head appearance.

14. Normal Brain
This is a normal brain with normal ridges called gyri and distinct depressions called sulci

15. Edematous Brain
When the edema of the brain is generalized either due to infection like encephalitis, trauma, obstruction to normal venous blood outflow we see the brain becomes grossly swollen with narrowed sulci and distended gyri. The brain takes on a flattened appearance as it presses against the unyielding skull.

17. Hyperemia and Congestion

18. Congestion and Hyperemia

19. CONGESTION AND HYPEREMIA

20. Congested Lungs
Patients who have heart failure develop pulmonary congestion and the gross cut surfaces are hemorrhagic and wet.

21. Acute Pulmonary Congestion
Microscopically we see the alveolar capillaries are engorged with blood there may some septal edema and focal intraalveolar hemorrhage.

22. “Heart Failure Cells” in Alveoli Chronic Pulmonary Congestion
In chronic pulmonary congestion the septa are much thickened and fibrotic and the alveolar spaces contain numerous hemosiderin laden macrophages due breakdown of red blood cells that extravasated into the alveolar spaces.

24. Congested and Enlarged Spleen
When blood cannot easily pass in the liver blood remains in the spleen. In this case the diminished outflow leads to a capillary bed swollen with deoxygenated venous blood and cyanosis.

25. Nutmeg liver

26. Microscopically, the nutmeg pattern results from congestion around the central veins, as seen here. This is usually due to a "right sided" heart failure.

27. Congested Liver (Passive) = Nutmeg Liver Right Heart Failure
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.; Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.

28. Hemorrhage

31. Here are petechial hemorrhages seen on the epicardium of the heart
Here are petechial hemorrhages seen on the epicardium of the heart. Petechiae (pinpoint hemorrhages) represent bleeding from small vessels and are classically found when a coagulopathy is due to a low platelet count. They can also appear following sudden hypoxia.

32. The blotchy areas of hemorrhage in the skin are called ecchymoses (singular ecchymosis), or also as areas of purpura. Ecchymoses are larger than petechiae. They can appear with coagulation disorders.

34. Intracerebral Hemorrhage
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.

35. Intracerebral Hemorrhage
This is a fatal intracerebral bleed. Even if the volumes of hemorrhage are small if they occur in a critical location or in a closed space like the brain it can have a fatal outcome.

36. Pericardial Hemorrhage

37. Hemostasis and Thrombosis

38. This is a schematic of the coag cascade
This is a schematic of the coag cascade. On the left is the intrinsic pathway which is initiated by activation of the Hagman factor- factor 12. The extrinsic pathway is on the right and is activated by tissue factor, a celluar lipoprotein exposed at sites of tissue injury. There is a common link betwn the intrinsic and extrinsic pathways at the level of factor X activation. Realize the division of the coag cascade is an artifact for in vitro testing. At the end there is a fibrin clot which forms to form a stable clot in the body.

39. THROMBOSIS -Virchow triad

40. Thrombus - Morphology Arterial Venous Arise in arteries
Grow in retrograde fashion (towards the heart- away from the direction of flow)
Forms at site of Endothelial injury (AS), turbulence (aneurysms)
Pale/ white
Lines of Zahn
Firmly adherent to vessel wall
From emboli  Cause infarctions (lower extremities – 75%, Brain, Kidney, spleen)
Venous
Arise in deep veins and superficial veins (popleteal  Femoral Iliac),
Antigrade (towards the heart- direction of flow)
At site of stasis (lower extremities)
Red / dark
No lines of Zahn
Loosely attached (easily embolize)
Emboli cause Pulmonary embolism ( silent in 50% of pts.)

41. These are "lines of Zahn" which are the alternating pale pink bands of platelets with fibrin and red bands of RBC's forming a true thrombus.

42. Venous Thrombi: Clinical

43. Thrombotic Vegetations Mitral Valve
Photo: Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.

44. Mural Thrombus
Here is an example of a mural thrombus which arises in the heart chamber and is adherent to the wall.
Usually dialated cardiomyopathy, MI or cardiac arrhythmias lead to the thrombus.

45. Abdominal Aortic Aneurysm Thrombus
In aortic aneurysms there is a saccular dilitation and an ulcerated atherosclerotic plaque which are a set up for an aortic thrombus.

46. Deep Vein Thrombosis (DVT)
This is a large leg vessel completely occluded by the large thrombosis.

47. Plaque with Recent Thrombus

48. Thrombosis Outcomes
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.

49. Early Organizing Thrombus

51. Embolism

52. Embolization (Embolus) Thromboembolism of Pulmonary Artery
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003; . Stevens A, Lowe J. Slide atlas of pathology. Mosby, London, 1995.

53. Right Ventricle Embolus from Leg Vein

54. Pulmonary Embolus

56. Infarction

57. Infarction (Infarct) Lung (Left); Spleen (Right)
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.

58. Pulmonary Infarction

59. Small Intestine Infarction

61. Kidney Infarction Replaced by Fibrotic Scar (Left)
Photo: Kumar, Cotran, Robbins. Robbins Basic pathology, 7th ed., Saunders, Philadelphia, 2003.

62. Pale Infarct (Wedge) of Spleen
The spleen, kidney and brain are examples of solid organs with end arterial circulation. Therefore these organs have pale infarcts and the density of the tissue limits the amount of hemorrhage that can seep into the ischemic area from adjoining capillary beds.