Atherosclerosis

Thromboangiitis Obliterans (Buerger

Disease)

Prof Dr Reetu Baral MD (Pathology)

Department of Pathology
Nobel Medical College Teaching Hospital
Atherosclerosis
Is characterized by intimal lesions called atheromas (or atheromatous or
atherosclerotic plaques) that impinge on the vascular lumen and can rupture to
cause sudden occlusion.
Atheromatous plaques are raised lesions composed of soft friable lipid cores
(mainly cholesterol and cholesterol esters, with necrotic debris) covered by fibrous
caps
Major Risk Factors for Atherosclerosis
1. Non-modifiable (Constitutional)
• Genetic abnormalities
• Family History
• Increasing age
• Male gender
2. Modifiable
• Hyperlipidemia
• Hypertension
• Cigarette smoking
• Diabetes
• Inflammation
Atherosclerosis: Pathogenesis

• Response-to-injury hypothesis.

• This model views atherosclerosis as a chronic inflammatory response

of the arterial wall to endothelial injury.

• Lesion progression involves interaction of:

• Modified lipoproteins
• Monocyte derived macrophages
• T lymphocytes
• The cellular constituents of the arterial wall
Atherosclerosis: Pathogenesis

• Endothelial Cell injury— results in

endothelial dysfunction— leading
to increased permeability, leukocyte
adhesion, and thrombosis
• Accumulation of lipoproteins
(mainly oxidized LDL and
cholesterol crystals) in the vessel
wall
• Platelet adhesion
• Monocyte adhesion to the
endothelium, migration into the
intima, and differentiation into
macrophages and foam cells
• Lipid accumulation within
macrophages, which respond by
releasing inflammatory cytokines
• Smooth muscle cell (SMC)
recruitment due to factors released
from activated platelets,
macrophages, and vascular wall
cells
• SMC proliferation and ECM
production
Morphology: Atherosclerosis
• Fatty Streaks:
• Begin as minute yellow, flat
macules that coalesce into
elongated lesions, 1 cm or more in
length
• They are composed of lipid-filled
foamy macrophages - minimally
raised and do not cause any
significant flow disturbance.
• Seen in infants younger than 1
year of age and are present in
virtually all children older than 10
years of age
Atherosclerotic Plaque
• Atheromatous plaques are white
to yellow raised lesions
• They range from 0.3 to 1.5 cm in
diameter but can form larger
masses
• The key features of these lesions
are intimal thickening and lipid
accumulation
• Thrombus superimposed on
ulcerated plaques imparts a red-
brown color
Vessels involved in Atherosclerosis
• In descending order of
severity, atherosclerosis
involves:
• Infra-renal abdominal aorta
• Coronary arteries
• Popliteal arteries
• Internal carotid arteries
• Vessels of the circle of Willis.
Atherosclerotic plaques

• Atherosclerotic plaques have three

principal components:

1. Cells:
• SMCs
• Macrophages
• T cells
2. ECM:
• Collagen
• Elastic fibers
• Proteoglycans
3. Lipid:
• Intracellular
• Extracellular
 Atherosclerotic plaque: clinically important changes
1. Rupture, ulceration, or erosion:
• Atheromatous plaques exposes
highly thrombogenic substances -
induces thrombus formation.
• Thrombi may partially or completely
occlude the lumen, leading to tissue
ischemia
2. Hemorrhage into a plaque:
• Intra-plaque hemorrhage -
hematoma - rapid plaque expansion
or plaque rupture
• Atheroembolism:
• Ruptured plaque can discharge debris
into the blood, producing
microemboli
• Aneurysm formation.
• Atherosclerosis-induced pressure or
ischemic atrophy of the underlying
media, with loss of elastic tissue,
causes structural weakening that can
lead to aneurysmal dilation and
rupture
Thromboangiitis obliterans (Buerger disease)

Occurs mainly in young men who

smoke

Inflammatory disease of peripheral

arteries resulting in the formation of
non-atherosclerotic lesions
 Digital, tibial, plantar, ulnar, and
palmar arteries

Obliterates the small and medium-

sized arteries
Dr. Reetu Baral
Thromboangiitis obliterans (Buerger disease)

Causes pain, tenderness,

and hair loss in the
affected area

Symptoms are caused by

slow, sluggish blood flow

Can often lead to

gangrenous lesions
Dr. Reetu Baral
Thromboangiitis obliterans (Buerger disease)

Dr. Reetu Baral

• The end
• Next class:
1. Aneurysm
2. Hypertension