QAMAR ASSISTANT PROFESSOR HISTOPATHOLOGY Athero sclerosis The atheroma lump of gruel from Greek athera meaning gruel OR Porridge Sclerosis means thickening Atherosclerosis ID: 774850
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Slide1
ATHEROSCLEROSIS
DR.SAMINA
QAMAR
ASSISTANT PROFESSOR
HISTOPATHOLOGY.
Slide2Athero-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 .
Slide3Arterioscelorosis
Slide4Also 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
.
Slide5Fatty streaks can appear in the aortas of infants younger than 1 year and are present in virtually all children older than 10 years.
Slide6Wall of artery showing fatty streaks/plaques.
Slide7Arteriosclerosis: Fatty streaks
Slide8Artery wall histology.
NORMAL ARTERY WALL
ARTERIOSCLEROTIC ARTERY WALL
Slide9What 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.
Slide10Consequences
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
.
Slide11Consequences.
Slide12Why it starts?
RISK FACTORS:
OLD AGE.MALE GENDER.POST MENOPAUSAL ESTROGEN DEFICIENCY.
Slide13RISK FACTORS
HYPERLIPIDEMIA(LDL).HYPERTENSION.OBESITY.CIGARETTE SMOKING.SEDENTRY LIFE STYLE.DIABETES.
Slide14HOW 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.
Slide15Participants
T-lymphocytes, monocytes/ Macrophages and normal constituents of arterial wall.
Slide16PATHOGENESIS.
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
Slide17How 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
Slide18AS
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.
Slide19PLAQUES: 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.
Slide20Atheroma is composed of
Slide21Atheroma.
Slide22Atheroma
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.
Slide23Histology of plaque.
Atheroma on the left. Cholesterol clefts are numerous in this atheroma. The surface on the far left shows ulceration and hemorrhage.
Slide24Slide25