1. Vascular Disorders

5. The white arrow on the black card marks the site of a ruptured berry aneurysm in the circle of Willis. This is a major cause of subarachnoid hemorrhage.

6. Arteriovenous Fistulas

7. The wall of this intramyocardial coronary artery is thickened and the lumen is narrowed due to abundant deranged muscle and fibrous tissue.

10. Hyaline arteriolosclerosis, which can be seen in patients with diabetes mellitus and with hypertension. This glomerulus stained with PAS shows nodular deposits of amorphous material (nodular glomerulosclerosis) along with a thickened arteriole at the lower right.

12. This is hyperplastic arteriolosclerosis, which most often appears in the kidney in patients with malignant hypertension. The arteriolar wall is markedly thickened and the lumen is narrowed.

13. Sometimes the small arteries and arterioles can be damaged so severely in malignant hypertension that they demonstrate necrosis with a pink fibrin-like quality that gives this process its name--fibrinoid necrosis.

15. Monckeberg's medial calcific sclerosis, which is the most insignificant form of arteriosclerosis (both atherosclerosis and arteriolosclerosis are definitely significant). Note the purplish blue calcifications in the media;

16. Atherosclerosis is a disease of the arteries in which fatty material is deposited in the vessel wall, resulting in narrowing and eventual impairment of blood flow. Severely restricted blood flow in the arteries to the heart muscle leads to symptoms such as chest pain. Atherosclerosis shows no symptoms until a complication occurs. atherosclerosis

22. The risk factors for atherosclerosis are diagrammed here in relation to the mechanisms that favor development of arterial atheroma formation.

27. Sequence of cellular interaction in atherosclerosis

31. The pale yellow lipid streaks in the aorta are the earliest lesion of atherosclerosis.

32. Three aortas are shown to demonstrate mild, moderate, and severe atherosclerosis from bottom to top.

33. This is mild coronary atherosclerosis. A few scattered yellow lipid plaques are seen on the intimal surface of the opened coronary artery traversing the epicardial surface of a heart. The degree of atherosclerosis here is not significant enough to cause disease, but could be the harbinger of worse atherosclerosis to come.

34. The plaques are formed of 1- Central core of cholesterol and cholesterol esters, lipid laden macrophages (foam cells), necrotic debris and calcification. 2- Subendothelial fibrous cap formed of proliferated smooth muscle cells, foam cells and extra cellular matrix

38. Grossly - Multiple irregular patches more around ostea of branches. - Color ranges from yellow to white according to relative amount of fat and fibrous tissue. - Covered by glistening intima (if not complicated)

41. Normal coronary artery with no atherosclerosis thrmbus

43. At higher magnification, many foam cells (macrophages full of lipid material) and a cholesterol cleft are seen in this atheromatous plaque. The plaque contains amorphous pink material with slit-like "cholesterol clefts" of lipid material. There is overlying recent hemorrhage at the left. Thrombus may form on top of such a plaque.

45. This is the gross appearance of severe coronary atherosclerosis, which involves virtually 100% of the surface of this coronary artery. There is extensive calcification, especially at the right where the lumen is narrowed. Calcification

46. The degree of atherosclerosis is much greater in this coronary artery, and the lumen is narrowed by half. A small area of calcification is seen in the plaque at the right.

47. Here is a coronary artery with atherosclerotic plaques. There is recent hemorrhage into the plaque. This is one of the complications of atherosclerosis. Such hemorrhage could acutely narrow the lumen and produce an acute coronary syndrome with ischemia and/or infarction of the myocardium. Hemorrhage

49. Thrombosis of the coronary artery Thrombosis on top of atheroma of the coronary artery

51. The Strokes

52. Peripheral Arterial Disease

69. Temporal Arteritis This figure is a high power view of a biopsy of a temporal artery in a subject with temporal arteritis. The black arrow demonstrates the endothelium with red blood cells in the intravascular space. The endothelium shows pathologic changes with edema and a proliferative subintimal response. The yellow arrow points out the disrupted elastic lamina and the blue arrow a granuloma typical of this form of large vessel vasculitis.

71. Takayasu’s arteritis showing fibrosis in all the layers of the vessel wall and markedly thickened intima (arrow)

74. Oral manifestations of Kawasaki disease: red lips and strawberry tongue.

75. Small coronary artery with segmental necrosis and inflammation in a patient with Kawasaki disease. Small coronary artery with segmental necrosis and inflammation in a patient with Kawasaki disease.

78. Thrombosed pseudoaneurysm in the pancreas of a patient with polyarteritis nodosa Renal involvement by polyarteritis nodosa. Note dark thrombosed pseudoaneurysms and pale peripheral infarc

80. Thromboangiites obliterans

81. Typical Acute Histologic Lesion of Buerger's Disease in a Vein with Intense Thromboangiitis, Showing a Microabscess in the Thrombus and Two Multinucleated Giant Cells

82. Wegener granulmatosis

83. Necrotizing granulomatous inflammation in the lung of a patient with Wegener's granulomatosis

85. Churg-Strauss Vasculitis The figure is a high power view of hematoxylin and eosin stained skin biopsy in a subject with Churg-Strauss vasculitis. The small blood vessel demonstrates findings of perivascular eosinophil infiltration (black arrows) of a small blood vessel wall, indicated by the white arrow head. These findings are similar to hypersensitivity vasculitis except for the predominance of eosinophils and involvement of both arterioles and venules.

86. Necrotizing and granulomatous arteritis in the lung of a patient with Churg-Strauss syndrome

87. Necrotizing glomerulonephritis with a cellular crescent, which may occur as a component of microscopic polyangiitis and other forms of small-vessel vasculitis.

88. Hypersensitivity Vasculitis This figure shows a low power view of hemotoxylin and eosin stained skin biopsy in a subject with hypersensitivity vasculitis. The biopsy demonstrates leukocytoclastic vasculitis. The black arrows point to small blood vessels in the subcutaneous tissue with perivascular leukocytes. A high power view would show blood cell extravasation and nuclear debris from lysed white blood cells (nuclear dust).

93. Massive pulmonary hemorrhage in a patient with Goodpasture's syndrome.

95. Esophageal varices with prominent red wale spots.

97. Cavernous Hemangioma at 10x Magnification

98. Histopathology of a proliferating infantile hemangioma with plump endothelial cells in the dermis. This superficial and deep infantile hemangioma resulted in astigmatism of the left eye

99. Capillary Hemangioma

100. Sinusoidal hemangioma. The vascular spaces are widely dilated.

102. Syphilitic Lymphadenitis Lymph Node in Secondary Syphilis : Newly formed blood vessels in the capsular and pericapsular regions show endothelial swelling and perivascular cuffs of plasma cells and lymphocytes. Prominent vasculitis is an important diagnostic clue in secondary syphilis