ATHEROSCLEROSIS
DR.SAMINA QAMAR
ASSISTANT 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 WALL
ARTERIOSCLEROTIC 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?
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RISK FACTORS:
OLD AGE.
MALE GENDER.
POST MENOPAUSAL
ESTROGEN DEFICIENCY.
RISK FACTORS
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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.