This document discusses atherosclerosis, a disease where plaque builds up inside arteries. It defines lipoproteins, which transport fats in the blood, and classifies different types based on density. The document then explains that atherosclerosis is caused by macrophages and fat accumulating in artery walls as plaques. These plaques can rupture, causing blood clots that block blood flow and lead to heart attacks or strokes. The progression of atherosclerosis involves endothelial dysfunction allowing LDL cholesterol to enter the artery wall and oxidative damage, followed by inflammation and plaque formation that narrows arteries over time.

1. ATHEROSCLEROSIS
Anushi Jain
Roll no. : 12
Paper I
MSc I

2. INTRODUCTION
• Any of a group of soluble proteins that combine
with and transport fat or other lipids in the
blood plasma are known as LIPOPROTEINS.
• Lipoproteins shows the presence of :
1. Triacyl Glycerol (TG)
2. Phospholipids (PL)
3. Cholesterol
4. Cholesterol Ester
5. A fraction of unesterified long chain fatty acid

3. • Lipoproteins are complete particles including :
1. A core consisting hydrophobic lipids ; such as,
TAG and cholesterol esters.
2. A surface monolayer of phospholipid,
cholesterol and hydrophilic amino acid side
chain forming surface protein
(apolipoprotein).

4. STRUCTURE OF LIPOPROTEIN

5. CLASSIFICATION OF LIPOPROTEINS
• Different combination of lipids and proteins
produce particles of different density as follows :
i. Chylomicron
ii. Very low density lipoprotein (VLDL)
iii. Intermediate Density lipoprotein (IDL)
iv. Low density lipoprotein (LDL)
v. High Density Lipoprotein (HDL)

6. ATHEROSCLEROSIS
• Atherosclerosis, the most common form of
arteriosclerosis (hardening of the arteries).
• It is also known as Arteriosclerotic Vascular Disease or
ASVD.
• It is characterized by the presence of atheromas,
arterial thickenings and depositing of pure
cholesteryl esters.
• Atherosclerosis is a progressive disease that begins as
intracellular lipid deposits in the smooth muscle cells of
the inner arterial wall. These lesions eventually become
fibrous, calcified plaques that narrow and even block
the arteries.

7. CAUSES
• Atherosclerosis is basically caused by
macrophages white blood cells and fat that
accumulate in arteries forming plaques.
• Atherosclerosis starts with damage or injury to
the inner layer of the artery. The factors that
triggers atherosclerosis include :
a. High blood pressure
b. High cholesterol
c. An irritant ; such as Nicotine
d. Certain diseases ; such as Diabetes

8. MECHANISM
• Atherosclerosis develops as a chronic
inflammatory responses of arterial walls to the
endothelial injury.
• Atherogenesis is the developmental process of
atheromatous plaques.
• It is characterized by a remodeling of arteries
leading to sub-endothelial accumulation of fatty
substances called plaques.

9. The Process Of Atherogenesis
A. Endothelial Dysfunction
• Early Atherogenesis is characterized by the
adherence of blood circulating white blood cell to
the vascular bed lining, the endothelium, then by
their migration to the sub-endothelial space, and
further activation into monocyte-derived
macrophages.
• Low density lipoprotein (LDL) in the blood invade
endothelium and gets oxidized by free radicals and
triggers inflammatory response.
• The WBC (monocytes) enters through blood
stream into endothelium and gets adhered there.

10. • The monocytes adhered to the endothelium
migrate across the endothelium. Once within the
arterial wall, the monocytes develop into
macrophages and begin to express scavenger
receptors.
• Scavenger receptors ingest oxidized LDL, slowly
turning into large "foam cells”, which is the
characteristic of lesions which then appears as
fatty streak.
• Foam cells eventually die, and further propagate
the inflammatory process.

12. B. Progression of inflammation to plaque
formation and expansion
• The progression of fatty streak into
atheromatous plaque occurs by the proliferation
of smooth muscle cells (SMC), their migration
and ingestion of lipids thus synthesis of collagen.
• A protective fibrous cap normally forms between
the fatty deposits and the artery lining.
• These capped fatty deposits (now called
'atheromas') produce enzymes that cause the
artery to enlarge over time forming atheromas
ulcers/plaques thus causing reduction in blood
flow .

13. Atheromas

15. C. Rupture
• When an atheromas ulcer/plaques ulcerates due
to over accumulation of the enzymes and fatty
deposits, it leads to immediate blood clotting at
the site of atheroma ulcer.
• This triggers a cascade of events that leads to
clot enlargement, which may quickly obstruct
the flow of blood.
• A complete blockage leads to ischemia of the
myocardial (heart) muscle and damage. This
process is the myocardial infarction or "heart
attack".

17. SYMPTOMS
• The first signs of atherosclerosis can begin to
develop during adolescence, with streaks of white
blood cells appearing on the artery wall. The
symptoms of the disease depend on which arteries
are affected:
A. Carotid Arteries
i. Weakness
ii. Difficulty breathing
iii. Headache
iv. Facial numbness
v. Paralysis

18. B. Coronary Arteries
i. Vomiting
ii. Extreme anxiety
iii. Chest pain
iv. Coughing
v. Feeling faint
C. Renal Arteries
i. Loss of appetite
ii. Swelling of the hands and feet
iii. Difficulty concentrating
D. Peripheral Arteries
i. Numbness
ii. Pain

19. DIAGNOSIS
• A diagnosis will be based on the medical history
of a patient, test results and a physical exam.
Diagnosis my include :
1. Blood Tests
2. Ultrasound
3. Electrocardiogram (ECG)
4. Computed Tomography (CT) scan
5. Ankle/Brachial Index

20. TREATMENT
• Treatments for atherosclerosis may
include heart-healthy
lifestyle changes, medicines, and medical
procedures or surgery.

21. THANK
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