ATHEROSCLEROSIS DR.SAMINA QAMAR ASSISTANT PROFESSOR HISTOPATHOLOGY

ATHEROSCLEROSIS

DR.SAMINA QAMARASSISTANT PROFESSOR

HISTOPATHOLOGY.

Athero-sclerosis

• The atheroma ("lump of gruel", from Greek (athera), meaning "gruel" OR Porridge.

• 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 .

Arterioscelorosis

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.

Fatty streaks can appear in the aortas of infants younger than 1 year and are present in virtually

all children older than 10 years.

Wall of artery showing fatty streaks/plaques.

Arteriosclerosis: Fatty streaks

Artery wall histology.

NORMAL ARTERY WALLARTERIOSCLEROTIC ARTERY WALL

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.

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.

• 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.

Consequences.

Why it starts?

• RISK FACTORS:• OLD AGE.• MALE GENDER.• POST MENOPAUSAL

ESTROGEN DEFICIENCY.

RISK FACTORS

• HYPERLIPIDEMIA(LDL).• HYPERTENSION.• OBESITY.• CIGARETTE SMOKING.• SEDENTRY LIFE STYLE.• DIABETES.

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.

Participants

• T-lymphocytes, monocytes/

• Macrophages and normal constituents of arterial wall.

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

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

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.

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.

Atheroma is composed of

Atheroma.

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.

Histology of plaque.

• Atheroma on the left. Cholesterol clefts are numerous in this atheroma. The surface on the far left shows ulceration and hemorrhage.