ATHEROSCLEROSISAnushi Jain

Roll no. : 12Paper I

MSc I

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. Cholesterol4. Cholesterol Ester5. A fraction of unesterified long chain

fatty acid

•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).

STRUCTURE OF LIPOPROTEIN

CLASSIFICATION OF LIPOPROTEINS

•Different combination of lipids and proteins produce particles of different density as follows :

i. Chylomicronii. Very low density lipoprotein (VLDL)iii. Intermediate Density lipoprotein (IDL)iv. Low density lipoprotein (LDL)v. High Density Lipoprotein (HDL)

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.

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 pressureb. High cholesterolc. An irritant ; such as Nicotined. Certain diseases ; such as Diabetes

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.

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.

•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.

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 .

Atheromas

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".

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 Arteriesi. Weaknessii. Difficulty breathing iii. Headache iv. Facial numbnessv. Paralysis

B. Coronary Arteriesi. Vomitingii. Extreme anxietyiii. Chest painiv. Coughingv. Feeling faintC. Renal Arteriesvi. Loss of appetitevii. Swelling of the hands and feetviii.Difficulty concentratingD. Peripheral Arteriesix. Numbnessx. Pain

DIAGNOSIS• A diagnosis will be based on the medical

history of a patient, test results and a physical exam. Diagnosis my include :

1. Blood Tests2. Ultrasound3. Electrocardiogram (ECG)4. Computed Tomography (CT) scan5. Ankle/Brachial Index

TREATMENT•Treatments for atherosclerosis may

include heart-healthy lifestyle changes, medicines, and medical procedures or surgery. 

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