This document discusses arteriosclerosis and atherosclerosis. It defines arteriosclerosis as hardening of the arteries, and identifies three patterns: small artery disease; calcification in aging muscular arteries; and atherosclerosis. Atherosclerosis is caused by fatty lesions called atheromas that protrude into arteries. Risk factors for atherosclerosis include age, gender, genetics, hyperlipidemia, hypertension, smoking, and diabetes. The pathogenesis involves endothelial injury, lipoprotein accumulation, monocyte recruitment, and smooth muscle cell proliferation. Morphologically, atherosclerosis begins as fatty streaks and progresses to atheromatous plaques containing lipids, cells, and extracellular matrix.

2. ARTERIOSCLEROSIS
BY
DR ABDUL AZIZ SHAIKH
MBBS,M.PHIL(HISTOPATHOLOGY)
LUMHS JAMSHORO

3. Consequences
ARTERIOSCLEROSIS
ATHEROSCLEROSIS:
EpidemiologyRisk factors
Pathogenesis
Morphology

4. Arteriosclerosis
means hardening of the arteries. It reflects arterial wall
thickening and loss of elasticity.
Three patterns.
a) Arteriosclerosis affects small arteries and arterioles
and cause ischemic injury.

5. b)Mönckeberg medial sclerosis
is calcific deposits in muscular arteries in old age.
c)Atheroclerossis:
Greek word for gruel and hardening.

6. ATHEROSCLEROSIS
•It is caused by intimal lesions called
atheromas that protude into vessel lumens.
•An atheromatous plaque consists of a raised
lesion with soft yellow, grumous core of
lipid(mainly cholesterol and cholesterol
esters) covered by a white fibrous cap.

8. ATHEROSCLEROSIS
•They cause obstruction of blood flow, can
rupture leading to catastrophic vessel
thrombosis, weakens media leads to
aneurysm formation.

9. EPIDEMIOLOGY
Constitutional risk factors in IHD:
a) Age: Old age
b) Gender: Females protected in pre menopausal age.
c) Genetics: Family History

10. CONTINUED
Modified risk Factors:
a) Hyperlipidemia: Hypercholestrolemia, LDL is bad
cholesterol.
b) Hypertension: Both systolic and diastolic
c) Cigarette smoking
d) Diabetes Mellitus

11. CONTINUED
Additional risk factors:
a) Inflammation: Increased CRP
b) Hyperhomocystinemia
c) Metabolic syndrome: Associated with insulin resistance
d) Lipoprotein (a) is an altered form of LDL
e) Factors affecting hemostasis: Elevated levels of
plasminogen activator inhibitor 1. Thrombin and platelet
derived factors.
f) Type A Personality persons

14. PATHOGENESIS
•Response-to-injury hypothesis: According to this,
atherosclerosis is a chronic inflammatory and
healing response of arterial wall to endothelial
injury.
•Lesion progression occurs through the interaction
of modified lipoproteins, monocyte-derived
macrophage, and T lymphocytes with the normal
cellular constituents arterial wall.

15. CONTINUED
Following Pathologic events occur:
a) Endothelial injury, which causes increased vascular
peremeability, leukocyte adhesion and thrombosis.
b) Accumulation of lipoproteins(mainly LDL) in the vessel
wall.
c) Monocyte adhesion to endothelium, followed by
migration into intima and transformation into
macrophages and foam cells.
d) Platelet adhesion

16. CONTINUED
e) Factor release from activated platelets,
macrophages and vascular wall cells inducing
smooth muscle cell recruitment.
f) Smooth muscle cell proliferation and ECM
production.
g) Lipid accumulation both extracellular and within
cells(macrophages and smooth muscles)

25. MORPHOLOGY
• Fatty streaks: Fatty streaks are the earliest lesion in
atherosclerosis. They are composed of lipid filled foamy
macrophages. These lesions don’t cause any flow
disturbane.
• Atherosclerotic plaque: The key processes in
atherosclerosis are intimal thickening and lipid
accumulation.
• Atheromatous plaque impinge on the lumen of artery and
grossly appear white to yellow; superimposed thrombus
over ulcerated plaques is red-brown.

26. ATHEROSCLEROTIC VESSEL

27. CONTINUED
Plaques vary from 0.3 to 1.5cm in diameter but
can coalese to form large masses.
 Atherosclerotic plaques have three principle
components.
i. Cells, including smooth muscle cells,
macrophages and T-cells.
ii. ECM including collagen, elastic fibers, and
proteoglycans and
iii. Intracellular and extra cellular lipid.

31. CONTINUED
Atherosclerotic plaques are susceptible to the
following clinically important changes.
i. Rupture, ulceration or erosin-leads to thrombosis
ii. Haemorrhage into a plaque.
iii. Atheroembolism.
iv. Aneurysm formation.

38. JAZAKALLAH