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aThERoSclERoSiS & aNEURYSMS

DR. Nashwah Al- Hariry


Lecturer of Pathology
Suez University
aThERoSclERoSiS
 Definition:
Patchy thickening of the intima of the arteries by
lesions composed of deposited lipids surrounded
by proliferated connective tissue. Those lesions
are called ATHEROMA
aThERoSclERoSiS
 Risk factors:
1. Hyperlipidemia (High level of plasma lipids):
• MAJOR risk factor.
2. Hypertention.
3. Stress.
4. Smoking, Alcohol.
5. Obesity.
6. Diabetes Mellitus.
7. Diet.
8. Age.
9. Sex: ↑ females ( after menopause) ..
10. Heredity: (Familial predisposition).
aThERoSclERoSiS
Pathogenesis
aThERoSclERoSiS
Pathogenesis
aThERoSclERoSiS
Pathogenesis
The most accepted theory is:
 Chronic endothelial injury ⇒ trapping of LDL in the
subendothelial part of the intima to which platelets, monocytes,
and lymphocytes adhere ⇒ release of cytokines (TNF, IL1) and
growth factors (eg., PDGF)

Macrophages that engulf LDL die and release oxidized LDL
+
Proliferation and migration of smooth muscle cells from media to
intima.

Intracellular and extracellular lipid to accumulate within plaque.
+
Proliferation of fibroblasts and extracellular matrix deposition
Common Sites:
 Large BV : Aorta, Carotid
& Iliac. (large arteries)
 Medium BV : Coronary,
Cerebral, Limbs.
 Small BV & Veins: Never
affected.
aThERoSclERoSiS
Morphologic types:

Fatty streaks F.Atheroma Plaques Complicated


aThERoSclERoSiS
ATHEROSCLEROSIS
Morpholoy
Gross Picture:
 Yellow streaks
 Atheromatous plaque
a- Fibrofatty plaque
b- Fibrous plaque
c- Complicated plaque:
 Calcification
 Fissuring and ulceration
 Superimposed thrombosis
 Haemorrhage
aThERoSclERoSiS
Morpholoy
:

A-Fatty streaks:
They are present early in life

 Site: Around aortic valve ring & thoracic aorta


 Gross: Thin, flat, yellow streaks in the intima
 M/E: Macrophages & SMCs distended with lipids
to form foam cells

Some streaks may progress to fibrous atheromatous


plaque
aThERoSclERoSiS
Morpholoy
B-Fibrous atheromatous plaque:
Site: Abdominal aorta at branching points
Medium sized arteries as coronary, carotid, basilar , renal ,mesenteric
and iliofemoral arteries
Gross: yellowish white elevated patches
M/E:
1- Fibrous cap : under the endothelium consisting of collagen, smcs,
and macrophages
2-Central Lipid zone : Foam cells (macrophages & smooth muscle
cells ) ,extracellular cholesterol crystals , lipids and necrotic debris
3- Basal zone : Smooth muscles and connective tissue
Fibro-fatty
plaque

Atheromatou
s
Plaque

Aortic atherosclerosis
aThERoSclERoSiS
Morpholoy
C- Complicated plaque
1- Thrombosis is the most common
2- Dystrophic calcification in the lipid zone
3- Ulceration of the endothelium ,so lipid contents discharged as
cholesterol emboli
4- Vascularization of the plaque leads to hemorrhage which expand it to
occlude the lumen
5- Aneurysms may develop in areas containing multiple plaques
Atheroma
Atheroma Aorta:
Atheroma Aorta:
Atheroma Coronary Artery:
Atheroma Coronary Artery:

Calcification
aThERoSclERoSiS
Effects and complications
1- AORTA:
- Atheromatous aneurysm; due to weakness of the media
- Mural thrombosis ► embolism
- Dissecting aneurysm due to fissuring of intima and media
2- Medium sized Arteries:
- Narrowing of the lumen ► Ischemia
- Thrombosis ► Infarction
- Aneurysmal dilatation
MoNckEbERg’S SclERoSiS
 Definition:
Calcification of the medium sized arteries of the medium
sized vessels.
Gross:
Hard rigid arterial wall without arterial lumen narrowing
+/- athersclerosis (in old age).
M/P:
Hyaline degeneration of the media + Patchy deposition of
calcium.
Clinical manifestations:
Insignificant (no luminal narrowing)
aRTERioSclERoSiS
Thickening and narrowing of the
small arteries occuring in
hypertention and diabetes mellitus
Arteriosclerosis Mockenberg’s Sclerosis
aNEURYSM
Localized abnormal dilation of the arterial wall. It may be:
True Aneurysm: i.e. the wall of the sac is formed by one or more layers
of affected vessel
False Aneurysm: formed of connective tissue around the vessel eg:
- Pulsating hematoma
- Arteriovenous fistula
TRUE aNEURYSMS
Morphological classification:
Fusiform
Saccular
Dissecting
Etiological classification:
 Congenital ; BERRY aneurysm , in circle of Willis at base of brain due
to congenital weakness of media. Rupture of it subarachnoid hemorrhage
 Atheromatous: in abdominal aorta, usually fusiform

 Dissecting ; common in the aorta


 Mycotic: due to infection & weakness in media e.g.
SIE, arteries in the wall of TB cavity,and abscesses
 Syphilitic ; in arch & ascending aorta , usually saccular
Aortic Berry
Aneurysm
Berry aneurysm
Berry Aneurysm:
TRUE aNEURYSMS
1-ATHEROSCLEROTIC ANEURYSMS
- The most common form of aortic aneurysms.,
- Commonly in males

 PATHOGENESIS :
Severe atherosclerotic lesions ►Thinning and destruction of the
medial elastic tissue ►Atrophy and weakening of the wall.

 EFFECTS
The clinical effects of atherosclerotic aneurysms are due to
complications:
1. Rupture
2. Compression
Atherosclerotic aneurysms
TRUE aNEURYSMS
2-DISSECTING ANEURYSMS
*The term dissecting aneurysm is applied for a dissecting
haematoma in which the blood enters the separated (dissected)
wall of the vessel .
*The most common site is the aorta .
*The condition commonly in old age , in men
* In women, dissecting aneurysms may occur during pregnancy.
TRUE aNEURYSMS
2-DISSECTING ANEURYSMS
PATHOGENESIS
weakened aortic media. Various conditions causing
weakening in the aortic wall resulting in dissection as :
i) Hypertensive state
About 90% cases of dissecting aneurysm have
hypertension.
ii) Non-hypertensive cases
These are cases due to some local or systemic connective
tissue disorder:
a) Marfan’s syndrome
b) Cystic medial necrosis
c) Iatrogenic trauma
d) Pregnancy
TRUE aNEURYSMS
2-DISSECTING ANEURYSMS

Effects:
1. HemopericardiumTIONS:
2. Mediastinal heemorrhage
3. Hemothorax
4. Abdominal hemorrhage
Dissecting aneurysm
Dissecting aneurysm
DISSECTING ANEURYSM

AORTA
DISSECTING
ANEURYSM

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