1. ATHEROSCLEROSIS DR.SAMINA QAMAR ASSISTANT PROFESSOR HISTOPATHOLOGY.

2. Athero-sclerosis The atheroma ("lump of gruel", from Greek (athera), meaning "gruel" OR Porridge.atheromaGreekgruel Sclerosis means thickening. Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a specific form of arteriosclerosis in which an arterial wall thickens as a result of invasion and accumulation of white blood cells.arteriosclerosis

3. Arterioscelorosis

4. Also called fatty streaks/plaques. Early on, Atheromas are called "fatty streaks“ because of yellow appearance due to collection of foam cells: fat containing macrophages. Later on the grumous core of lipid is covered by a white fibrous cap and then its called an atheroma.

5. Fatty streaks can appear in the aortas of infants younger than 1 year and are present in virtually all children older than 10 years.

6. Wall of artery showing fatty streaks/plaques.

7. Arteriosclerosis: Fatty streaks

8. Artery wall histology. NORMAL ARTERY WALL ARTERIOSCLEROTIC ARTERY WALL

9. What are the results of atherosclerosis? These changes reduce the elasticity of the arterial wall but do not affect blood flow for decades because the muscular wall of artery enlarges at the locations of plaque. Atherosclerotic lesions can cause thromboembolism and complete closure of the lumen of a small blood vessel.

10. Consequences Atheroma can suddenly rupture, causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately 5 minutes.thrombus If artery of heart is blocked it can cause a heart attack. The same process in an artery to the brain is commonly called stroke.stroke

11. Consequences.

12. Why it starts? RISK FACTORS: OLD AGE. MALE GENDER. POST MENOPAUSAL ESTROGEN DEFICIENCY.

13. RISK FACTORS HYPERLIPIDEMIA(LDL). HYPERTENSION. OBESITY. CIGARETTE SMOKING. SEDENTRY LIFE STYLE. DIABETES.

14. HOW IT STARTS? Response-to-injury hypothesis This model views atherosclerosis as a chronic inflammatory response of the arterial wall to endothelial injury. Hemodynamic disturbances, toxins and hypercholesterolemia.

15. Participants T-lymphocytes, monocytes/ Macrophages and normal constituents of arterial wall.

16. PATHOGENESIS. 1-After endothelial injury monocytes cluster beneath endothelium. 2-Macrophages,foam cells and platelets also accumulate. 3- They start engulfing lipid intracellulary. 4- SMC and collagen are deposited. 5-Extracellular lipid is released

17. How do they appear grossly? Atheromatous plaques grossly appear white to yellow. Thrombosis superimposed over the surface of ulcerated plaques is red-brown in color. Plaques vary from 0.3 to 1.5 cm in diameter but can coalesce to form larger masses

18. AS Mild AS : scattered lipid plaques. Middle: shows many more larger plaques. The severe atherosclerosis in the aorta at the top shows extensive ulceration in the plaques.

19. PLAQUES: C,E,L. Atherosclerotic plaques have three principal components: (1)Cells: SMCs, macrophages, and T cells. (2)ECM: collagen, elastic fibers, and proteoglycans. (3)Lipid: intracellular and extracellular.

20. Atheroma is composed of

21. Atheroma.

22. Atheroma Superficial fibrous cap is composed of SMCs and relatively dense collagen. Beneath and to the side of the cap (the "shoulder") is a more cellular area containing macrophages, T cells, and SMCs. Deep to the fibrous cap is a necrotic core, containing lipid (primarily cholesterol and cholesterol esters), debris from dead cells, foam cells (lipid-laden macrophages and SMCs), fibrin, plasma proteins and the cholesterol that appears as clefts.

23. Histology of plaque. Atheroma on the left. Cholesterol clefts are numerous in this atheroma. The surface on the far left shows ulceration and hemorrhage.