DRSAMINA QAMAR ASSISTANT PROFESSOR HISTOPATHOLOGY Athero sclerosis The atheroma lump of gruel from Greek athera meaning gruel OR Porridge Sclerosis means thickening ID: 367281
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Slide1
ATHEROSCLEROSIS
DR.SAMINA
QAMAR
ASSISTANT PROFESSOR
HISTOPATHOLOGY.Slide2
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 .Slide3
ArterioscelorosisSlide4
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
.Slide5
Fatty streaks can appear in the aortas of infants younger than 1 year and are present in virtually all children older than 10 years
.Slide6
Wall of artery showing fatty streaks/plaques.Slide7
Arteriosclerosis: Fatty streaksSlide8
Artery wall histology.
NORMAL ARTERY WALL
ARTERIOSCLEROTIC ARTERY WALLSlide9
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.Slide10
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
.Slide11
Consequences.Slide12
Why it starts?
RISK FACTORS:
OLD AGE.
MALE GENDER.
POST MENOPAUSAL ESTROGEN DEFICIENCY.Slide13
RISK FACTORS
HYPERLIPIDEMIA(LDL).
HYPERTENSION.
OBESITY.
CIGARETTE SMOKING.
SEDENTRY LIFE STYLE.
DIABETES.Slide14
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.Slide15
Participants
T-lymphocytes,
monocytes
/
Macrophages and normal constituents of arterial wall.Slide16
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 releasedSlide17
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 Slide18
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.Slide19
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.Slide20
Atheroma is composed ofSlide21
Atheroma.Slide22
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.Slide23
Histology of plaque.
Atheroma
on the left. Cholesterol clefts are numerous in this
atheroma
. The surface on the far left shows ulceration and hemorrhage. Slide24Slide25