atherosclerosis dr.samina qamar assistant professor histopathology
TRANSCRIPT
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.