SlideShare a Scribd company logo

Atherosclerosis

•Download as PPTX, PDF•
•
Anushi Jain
Anushi Jain

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.

Convert to study guideBETA

Transform any presentation into a summarized study guide, highlighting the most important points and key insights.

1 of 21
Downloaded 120 times
ATHEROSCLEROSIS Anushi Jain Roll no. : 12 Paper 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. Cholesterol 4. Cholesterol Ester 5. 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. Chylomicron ii. 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 pressure b. High cholesterol c. An irritant ; such as Nicotine d. 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.
Atherosclerosis
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
Atherosclerosis
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".
Atherosclerosis
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
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
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
TREATMENT • Treatments for atherosclerosis may include heart-healthy lifestyle changes, medicines, and medical procedures or surgery.
THANK YOU

More Related Content

Atherosclerosis

  • 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).
  • 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 .
  • 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.