{"id":5595,"date":"2025-12-13T14:46:42","date_gmt":"2025-12-13T19:46:42","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=5595"},"modified":"2026-01-12T18:33:44","modified_gmt":"2026-01-12T23:33:44","slug":"atherosclerosis-and-atheromas","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/atherosclerosis-and-atheromas\/","title":{"raw":"7p19  Atherosclerosis and Atheromas","rendered":"7p19  Atherosclerosis and Atheromas"},"content":{"raw":"<strong>Atherosclerosis and Atheromas<\/strong>\r\n<h1><strong>Definitions of Atherosclerosis and Atheroma:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Atherosclerosis<\/strong>\u00a0specifically refers to the development of\u00a0<strong>atheromas<\/strong>\u00a0or\u00a0<strong>atherosclerotic plaques<\/strong>\u00a0within arterial walls.<\/li>\r\n<\/ul>\r\n<h1><strong>Composition of Plaques:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Mostly\u00a0<strong>fat<\/strong>\u00a0deposits.<\/li>\r\n \t<li>Contains\u00a0<strong>calcium<\/strong>\u00a0(dystrophic calcification in damaged tissue).<\/li>\r\n \t<li>May include\u00a0<strong>fibrin<\/strong>,\u00a0<strong>thrombus material<\/strong>,\u00a0<strong>cellular debris<\/strong>,\u00a0<strong>red and white blood cells<\/strong>.<\/li>\r\n \t<li>These components cluster together, creating a\u00a0<strong>mass<\/strong>\u00a0or plaque.<\/li>\r\n<\/ul>\r\n<h1><strong>Most Susceptible Vessels:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Large arteries<\/strong>, including:\r\n<ul>\r\n \t<li><strong>Aorta<\/strong><\/li>\r\n \t<li><strong>Iliac arteries<\/strong><\/li>\r\n \t<li><strong>Coronary arteries<\/strong>\u00a0(heart)<\/li>\r\n \t<li><strong>Carotid arteries<\/strong>\u00a0(brain)<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Points of bifurcation:<\/strong>\r\n<ul>\r\n \t<li>Where a vessel forks or splits into two branches, causing <strong>turbulence<\/strong>\u00a0and\u00a0<strong>shear stress<\/strong>.<\/li>\r\n \t<li>Turbulence damages vessel walls, favoring plaque formation at these sites.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Impact of plaques:<\/strong><\/h1>\r\n<ul>\r\n \t<li>Reduced blood flow leads to\u00a0<strong>impaired muscle activity<\/strong>\u00a0and\u00a0<strong>nerve function<\/strong>.<\/li>\r\n \t<li>Causes\u00a0<strong>ischemia<\/strong>\u2014tissue damage due to lack of oxygen.<\/li>\r\n \t<li>Precipitated by\u00a0<strong>damage<\/strong>\u00a0to vessel walls at bifurcations.<\/li>\r\n<\/ul>\r\n<h1><strong>Risk Factors &amp; Lifestyle:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Diet:<\/strong>\u00a0Fat, salt, and cholesterol intake.<\/li>\r\n \t<li><strong>Exercise:<\/strong>\u00a0Sedentary lifestyles increase risk.<\/li>\r\n \t<li><strong>Stress:<\/strong>\u00a0Chronic stress contributes to endothelial damage.<\/li>\r\n \t<li><strong>Nature of damage:<\/strong>\u00a0Daily stress and chronic stress accelerate plaque formation.<\/li>\r\n<\/ul>\r\n<h1><strong>Medical Interventions:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Endarterectomy:<\/strong>\u00a0Surgical removal of plaques from blood vessel walls, often at bifurcations like the carotids.<\/li>\r\n<\/ul>\r\n<h1><strong>Visuals:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Normal aorta:<\/strong>\u00a0Smooth, unblocked, laminar blood flow.<\/li>\r\n \t<li><strong>Atherosclerotic aorta:<\/strong>\u00a0Plaque buildup, causing irregularities and turbulence, which further damages vessel walls and promotes plaque growth.<\/li>\r\n \t<li><strong>Downstream damage:<\/strong>\u00a0Turbulence propagates stress and injury to smaller arteries downstream.<\/li>\r\n<\/ul>\r\n<h1><strong>Lipids and Lipoproteins in Atherosclerosis<\/strong><\/h1>\r\n<strong>Sources of Lipids:<\/strong>\r\n<ul>\r\n \t<li><strong>LDL (Low-Density Lipoprotein):<\/strong>\r\n<ul>\r\n \t<li>Produced by the liver to\u00a0<strong>transport lipids<\/strong>\u00a0(mainly cholesterol and triglycerides) to cells.<\/li>\r\n \t<li>Essential because lipid is an\u00a0<strong>energy source<\/strong>\u00a0and a\u00a0<strong>building block<\/strong>\u00a0for cell membranes and hormones.<\/li>\r\n \t<li>However, LDL particles are\u00a0<strong>\"sloppy\"<\/strong>, meaning their lipid cargo can\u00a0<strong>accumulate in blood vessel walls<\/strong>, forming atheromas.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong>Lipoprotein Functions:<\/strong>\r\n<ul>\r\n \t<li><strong>HDL (High-Density Lipoprotein):<\/strong>\r\n<ul>\r\n \t<li>Known as the\u00a0<strong>scavenger<\/strong>\u00a0lipoprotein.<\/li>\r\n \t<li>Collects excess\u00a0<strong>cholesterol<\/strong>\u00a0and\u00a0<strong>lipids<\/strong>\u00a0coming from LDL.<\/li>\r\n \t<li>Returns these lipids to the liver for\u00a0<strong>metabolism, energy production,<\/strong>\u00a0or\u00a0<strong>bile formation<\/strong>\u00a0for excretion.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Lipid Metabolism Pathway, HDLs and LDLs:<\/strong><\/h1>\r\n<ul>\r\n \t<li><strong>Dietary fats:<\/strong>\r\n<ul>\r\n \t<li>Cholesterol and triglycerides are ingested with food.<\/li>\r\n \t<li>The intestine\u00a0<strong>breaks down<\/strong>\u00a0fats into smaller molecules, which are\u00a0<strong>absorbed into the bloodstream<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Transport:<\/strong>\r\n<ul>\r\n \t<li>Lipids are\u00a0<strong>water-insoluble<\/strong>, so they are\u00a0<strong>packed into vesicles<\/strong>\u00a0called lipoproteins with\u00a0<strong>proteins<\/strong>\u00a0for transport.<\/li>\r\n \t<li>These vesicles travel to tissues like\u00a0<strong>skeletal muscle<\/strong>\u00a0(active, needing energy) and\u00a0<strong>adipose tissue<\/strong>\u00a0(storage, insulation, cushioning).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Liver processing:<\/strong>\r\n<ul>\r\n \t<li>Lipids reaching the liver are\u00a0<strong>packaged as LDL<\/strong>\u2014<strong>\"sloppy\"<\/strong>\u00a0and rich in lipids (~75% lipid content).<\/li>\r\n \t<li>LDL particles bind to\u00a0<strong>LDL receptors<\/strong>\u00a0on\u00a0<strong>endothelial and smooth muscle cells<\/strong>\u00a0lining blood vessels.<\/li>\r\n \t<li>Excess LDL uptake in vessel walls leads to\u00a0<strong>lipid accumulation<\/strong>\u00a0and formation of\u00a0<strong>atherosclerotic plaques<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong>Role of HDL:<\/strong>\r\n<ul>\r\n \t<li>Acts as\u00a0<strong>scavenger<\/strong>: retrieves excess lipids from blood vessel walls.<\/li>\r\n \t<li>Returns lipids to the liver for\u00a0<strong>breakdown<\/strong>\u00a0and\u00a0<strong>excretion<\/strong>.<\/li>\r\n<\/ul>\r\n<strong>Visual Summary (Pie Charts):<\/strong>\r\n<ul>\r\n \t<li><strong>HDL (High-density lipoprotein):<\/strong>\u00a0~50% protein, ~50% lipid (cholesterol, triglycerides, phospholipids).<\/li>\r\n \t<li><strong>LDL (Low-density lipoprotein):<\/strong>\u00a0&gt;75% lipid content, very \"sloppy\" and prone to depositing lipids in vessel walls.<\/li>\r\n<\/ul>\r\n<h1><strong>Pathogenesis of Atherosclerosis:<\/strong><\/h1>\r\n<ol>\r\n \t<li><strong>Initial Step:<\/strong> <strong>Endothelial injury<\/strong>\u2014damage to the innermost layer (tunica intima) of blood vessels.\r\n<ul>\r\n \t<li><strong>Causes of damage:<\/strong>\r\n<ul>\r\n \t<li><strong>Hypertension:<\/strong>\u00a0Elevated pressure damages vessel walls.<\/li>\r\n \t<li><strong>Smoking:<\/strong>\u00a0Damages endothelial cells, increases oxidative stress.<\/li>\r\n \t<li><strong>Hyperlipidemia:<\/strong>\u00a0Excess lipids infiltrate the damaged endothelium.<\/li>\r\n \t<li><strong>Genetic factors:<\/strong>\u00a0Increased lipid production or receptor activity.<\/li>\r\n \t<li><strong>Other factors:<\/strong>\u00a0High homocysteine, turbulent flow at bifurcations, toxins, infections, immune reactions, virus-induced damage.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Inflammation Response:<\/strong>\r\n<ul>\r\n \t<li>Increased\u00a0<strong>C-reactive protein (CRP)<\/strong>\u00a0as a marker of inflammation.<\/li>\r\n \t<li>Attraction of\u00a0<strong>white blood cells<\/strong>: monocytes and macrophages.<\/li>\r\n \t<li>Macrophages ingest lipids and become\u00a0<strong>foamy macrophages<\/strong>\u00a0(foam cells).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Plaque Formation:<\/strong><\/li>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Lipids embed into the damaged endothelial space.<\/li>\r\n \t<li>Platelets adhere, activate, and form a\u00a0<strong>thrombus<\/strong>.<\/li>\r\n \t<li><strong>Smooth muscle proliferation<\/strong>\u00a0and\u00a0<strong>fibroblast<\/strong>\u00a0activity lead to collagen deposition, forming a\u00a0<strong>fibrous cap<\/strong>\u00a0over the plaque.<\/li>\r\n \t<li>Plaque can\u00a0<strong>calcify<\/strong>, making it more rigid, less elastic, and prone to\u00a0<strong>fissures<\/strong>\u00a0or rupture.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Progression:<\/strong>\r\n<ul>\r\n \t<li>Plaques grow larger,\u00a0<strong>narrowing the lumen<\/strong>.<\/li>\r\n \t<li>Leukocyte, platelet, and lipid accumulation worsen the obstruction.<\/li>\r\n \t<li>Turbulence from plaque causes further endothelial injury downstream, creating a\u00a0<strong>vicious cycle<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong> Consequences of Plaque Development:<\/strong><\/li>\r\n<\/ol>\r\n<ul>\r\n \t<li>Reduced blood flow causes\u00a0<strong>ischemia<\/strong>.<\/li>\r\n \t<li>Plates and thrombi can\u00a0<strong>embolize<\/strong>, leading to downstream blockages.<\/li>\r\n \t<li>Plaque rupture can trigger\u00a0<strong>acute events<\/strong>\u00a0like\u00a0<strong>heart attack<\/strong>\u00a0or\u00a0<strong>stroke<\/strong>.<\/li>\r\n<\/ul>\r\n<h1><strong>Risk Factors:<\/strong><\/h1>\r\n<table class=\"grid landscape\">\r\n<thead>\r\n<tr class=\"shaded\">\r\n<td><strong>Type<\/strong><\/td>\r\n<td><strong>Factors<\/strong><\/td>\r\n<td><strong>Description<\/strong><\/td>\r\n<\/tr>\r\n<\/thead>\r\n<tbody>\r\n<tr>\r\n<td><strong>Non-modifiable<\/strong><\/td>\r\n<td>Age, being male, genetic predisposition<\/td>\r\n<td>Can't be changed; age-related plaque buildup common.<\/td>\r\n<\/tr>\r\n<tr>\r\n<td><strong>Modifiable<\/strong><\/td>\r\n<td>Obesity, smoking, sedentary lifestyle, poor diet, diabetes, hypertension, hormone therapy + smoking<\/td>\r\n<td>Lifestyle and health factors influencing plaque development.<\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n<ul>\r\n \t<li><strong>Smoking:<\/strong>\r\n<ul>\r\n \t<li>Decreases\u00a0<strong>HDL (\"good\" cholesterol)<\/strong>, increases\u00a0<strong>LDL (\"bad\" cholesterol)<\/strong>.<\/li>\r\n \t<li>Promotes\u00a0<strong>vasoconstriction<\/strong>\u00a0and\u00a0<strong>platelet adhesion<\/strong>, increasing clot risk.<\/li>\r\n \t<li>Raises\u00a0<strong>heart rate<\/strong>\u00a0and\u00a0<strong>blood pressure<\/strong>.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Diabetes:<\/strong>\r\n<ul>\r\n \t<li>Elevates\u00a0<strong>glucose and lipid levels<\/strong>, damaging endothelium, promoting plaques.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Hypertension:<\/strong>\r\n<ul>\r\n \t<li>Causes\u00a0<strong>endothelial injury<\/strong>, accelerating plaque formation.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Combination factors:<\/strong>\r\n<ul>\r\n \t<li>Use of\u00a0<strong>birth control pills<\/strong>\u00a0combined with\u00a0<strong>smoking<\/strong>\u00a0especially after age 35 greatly increases clotting risk.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<h1><strong>Summary:<\/strong><\/h1>\r\n<strong>Atherosclerosis<\/strong> involves fatty deposits causing vessel narrowing and turbulence, leading to progressive damage and risk of infarction.\r\n\r\n<strong>Large arteries<\/strong> such as the <strong>aorta<\/strong> and <strong>coronary arteries<\/strong> are particularly vulnerable, and lifestyle factors heavily influence plaque development.\r\n\r\n<strong>Key Concepts:<\/strong>\r\n<ul>\r\n \t<li><strong>LDL:<\/strong>\u00a0Delivers lipids but can promote plaque buildup if levels are high.<\/li>\r\n \t<li><strong>HDL:<\/strong>\u00a0Protects against atherosclerosis by cleaning up excess lipids.<\/li>\r\n \t<li>Managing lipid levels through diet, activity, and medications helps prevent or slow the progression of atherosclerosis.<\/li>\r\n<\/ul>\r\n<strong>Atherosclerosis<\/strong> begins with <strong>endothelial injury<\/strong> and progression involves <strong>lipid accumulation<\/strong>, <strong>inflammation,<\/strong> and <strong>plaque formation<\/strong>.\r\n\r\nLifestyle factors like <strong>smoking, diet,<\/strong> and <strong>inactivity<\/strong> significantly influence disease progression, while medical interventions aim to prevent or remove plaques and reduce the risk of acute cardiovascular events.\r\n\r\nSurgical removal of plaques is possible, but <strong>prevention<\/strong> remains key.","rendered":"<p><strong>Atherosclerosis and Atheromas<\/strong><\/p>\n<h1><strong>Definitions of Atherosclerosis and Atheroma:<\/strong><\/h1>\n<ul>\n<li><strong>Atherosclerosis<\/strong>\u00a0specifically refers to the development of\u00a0<strong>atheromas<\/strong>\u00a0or\u00a0<strong>atherosclerotic plaques<\/strong>\u00a0within arterial walls.<\/li>\n<\/ul>\n<h1><strong>Composition of Plaques:<\/strong><\/h1>\n<ul>\n<li>Mostly\u00a0<strong>fat<\/strong>\u00a0deposits.<\/li>\n<li>Contains\u00a0<strong>calcium<\/strong>\u00a0(dystrophic calcification in damaged tissue).<\/li>\n<li>May include\u00a0<strong>fibrin<\/strong>,\u00a0<strong>thrombus material<\/strong>,\u00a0<strong>cellular debris<\/strong>,\u00a0<strong>red and white blood cells<\/strong>.<\/li>\n<li>These components cluster together, creating a\u00a0<strong>mass<\/strong>\u00a0or plaque.<\/li>\n<\/ul>\n<h1><strong>Most Susceptible Vessels:<\/strong><\/h1>\n<ul>\n<li><strong>Large arteries<\/strong>, including:\n<ul>\n<li><strong>Aorta<\/strong><\/li>\n<li><strong>Iliac arteries<\/strong><\/li>\n<li><strong>Coronary arteries<\/strong>\u00a0(heart)<\/li>\n<li><strong>Carotid arteries<\/strong>\u00a0(brain)<\/li>\n<\/ul>\n<\/li>\n<li><strong>Points of bifurcation:<\/strong>\n<ul>\n<li>Where a vessel forks or splits into two branches, causing <strong>turbulence<\/strong>\u00a0and\u00a0<strong>shear stress<\/strong>.<\/li>\n<li>Turbulence damages vessel walls, favoring plaque formation at these sites.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Impact of plaques:<\/strong><\/h1>\n<ul>\n<li>Reduced blood flow leads to\u00a0<strong>impaired muscle activity<\/strong>\u00a0and\u00a0<strong>nerve function<\/strong>.<\/li>\n<li>Causes\u00a0<strong>ischemia<\/strong>\u2014tissue damage due to lack of oxygen.<\/li>\n<li>Precipitated by\u00a0<strong>damage<\/strong>\u00a0to vessel walls at bifurcations.<\/li>\n<\/ul>\n<h1><strong>Risk Factors &amp; Lifestyle:<\/strong><\/h1>\n<ul>\n<li><strong>Diet:<\/strong>\u00a0Fat, salt, and cholesterol intake.<\/li>\n<li><strong>Exercise:<\/strong>\u00a0Sedentary lifestyles increase risk.<\/li>\n<li><strong>Stress:<\/strong>\u00a0Chronic stress contributes to endothelial damage.<\/li>\n<li><strong>Nature of damage:<\/strong>\u00a0Daily stress and chronic stress accelerate plaque formation.<\/li>\n<\/ul>\n<h1><strong>Medical Interventions:<\/strong><\/h1>\n<ul>\n<li><strong>Endarterectomy:<\/strong>\u00a0Surgical removal of plaques from blood vessel walls, often at bifurcations like the carotids.<\/li>\n<\/ul>\n<h1><strong>Visuals:<\/strong><\/h1>\n<ul>\n<li><strong>Normal aorta:<\/strong>\u00a0Smooth, unblocked, laminar blood flow.<\/li>\n<li><strong>Atherosclerotic aorta:<\/strong>\u00a0Plaque buildup, causing irregularities and turbulence, which further damages vessel walls and promotes plaque growth.<\/li>\n<li><strong>Downstream damage:<\/strong>\u00a0Turbulence propagates stress and injury to smaller arteries downstream.<\/li>\n<\/ul>\n<h1><strong>Lipids and Lipoproteins in Atherosclerosis<\/strong><\/h1>\n<p><strong>Sources of Lipids:<\/strong><\/p>\n<ul>\n<li><strong>LDL (Low-Density Lipoprotein):<\/strong>\n<ul>\n<li>Produced by the liver to\u00a0<strong>transport lipids<\/strong>\u00a0(mainly cholesterol and triglycerides) to cells.<\/li>\n<li>Essential because lipid is an\u00a0<strong>energy source<\/strong>\u00a0and a\u00a0<strong>building block<\/strong>\u00a0for cell membranes and hormones.<\/li>\n<li>However, LDL particles are\u00a0<strong>&#8220;sloppy&#8221;<\/strong>, meaning their lipid cargo can\u00a0<strong>accumulate in blood vessel walls<\/strong>, forming atheromas.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong>Lipoprotein Functions:<\/strong><\/p>\n<ul>\n<li><strong>HDL (High-Density Lipoprotein):<\/strong>\n<ul>\n<li>Known as the\u00a0<strong>scavenger<\/strong>\u00a0lipoprotein.<\/li>\n<li>Collects excess\u00a0<strong>cholesterol<\/strong>\u00a0and\u00a0<strong>lipids<\/strong>\u00a0coming from LDL.<\/li>\n<li>Returns these lipids to the liver for\u00a0<strong>metabolism, energy production,<\/strong>\u00a0or\u00a0<strong>bile formation<\/strong>\u00a0for excretion.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Lipid Metabolism Pathway, HDLs and LDLs:<\/strong><\/h1>\n<ul>\n<li><strong>Dietary fats:<\/strong>\n<ul>\n<li>Cholesterol and triglycerides are ingested with food.<\/li>\n<li>The intestine\u00a0<strong>breaks down<\/strong>\u00a0fats into smaller molecules, which are\u00a0<strong>absorbed into the bloodstream<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Transport:<\/strong>\n<ul>\n<li>Lipids are\u00a0<strong>water-insoluble<\/strong>, so they are\u00a0<strong>packed into vesicles<\/strong>\u00a0called lipoproteins with\u00a0<strong>proteins<\/strong>\u00a0for transport.<\/li>\n<li>These vesicles travel to tissues like\u00a0<strong>skeletal muscle<\/strong>\u00a0(active, needing energy) and\u00a0<strong>adipose tissue<\/strong>\u00a0(storage, insulation, cushioning).<\/li>\n<\/ul>\n<\/li>\n<li><strong>Liver processing:<\/strong>\n<ul>\n<li>Lipids reaching the liver are\u00a0<strong>packaged as LDL<\/strong>\u2014<strong>&#8220;sloppy&#8221;<\/strong>\u00a0and rich in lipids (~75% lipid content).<\/li>\n<li>LDL particles bind to\u00a0<strong>LDL receptors<\/strong>\u00a0on\u00a0<strong>endothelial and smooth muscle cells<\/strong>\u00a0lining blood vessels.<\/li>\n<li>Excess LDL uptake in vessel walls leads to\u00a0<strong>lipid accumulation<\/strong>\u00a0and formation of\u00a0<strong>atherosclerotic plaques<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong>Role of HDL:<\/strong><\/p>\n<ul>\n<li>Acts as\u00a0<strong>scavenger<\/strong>: retrieves excess lipids from blood vessel walls.<\/li>\n<li>Returns lipids to the liver for\u00a0<strong>breakdown<\/strong>\u00a0and\u00a0<strong>excretion<\/strong>.<\/li>\n<\/ul>\n<p><strong>Visual Summary (Pie Charts):<\/strong><\/p>\n<ul>\n<li><strong>HDL (High-density lipoprotein):<\/strong>\u00a0~50% protein, ~50% lipid (cholesterol, triglycerides, phospholipids).<\/li>\n<li><strong>LDL (Low-density lipoprotein):<\/strong>\u00a0&gt;75% lipid content, very &#8220;sloppy&#8221; and prone to depositing lipids in vessel walls.<\/li>\n<\/ul>\n<h1><strong>Pathogenesis of Atherosclerosis:<\/strong><\/h1>\n<ol>\n<li><strong>Initial Step:<\/strong> <strong>Endothelial injury<\/strong>\u2014damage to the innermost layer (tunica intima) of blood vessels.\n<ul>\n<li><strong>Causes of damage:<\/strong>\n<ul>\n<li><strong>Hypertension:<\/strong>\u00a0Elevated pressure damages vessel walls.<\/li>\n<li><strong>Smoking:<\/strong>\u00a0Damages endothelial cells, increases oxidative stress.<\/li>\n<li><strong>Hyperlipidemia:<\/strong>\u00a0Excess lipids infiltrate the damaged endothelium.<\/li>\n<li><strong>Genetic factors:<\/strong>\u00a0Increased lipid production or receptor activity.<\/li>\n<li><strong>Other factors:<\/strong>\u00a0High homocysteine, turbulent flow at bifurcations, toxins, infections, immune reactions, virus-induced damage.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<li><strong>Inflammation Response:<\/strong>\n<ul>\n<li>Increased\u00a0<strong>C-reactive protein (CRP)<\/strong>\u00a0as a marker of inflammation.<\/li>\n<li>Attraction of\u00a0<strong>white blood cells<\/strong>: monocytes and macrophages.<\/li>\n<li>Macrophages ingest lipids and become\u00a0<strong>foamy macrophages<\/strong>\u00a0(foam cells).<\/li>\n<\/ul>\n<\/li>\n<li><strong>Plaque Formation:<\/strong><\/li>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Lipids embed into the damaged endothelial space.<\/li>\n<li>Platelets adhere, activate, and form a\u00a0<strong>thrombus<\/strong>.<\/li>\n<li><strong>Smooth muscle proliferation<\/strong>\u00a0and\u00a0<strong>fibroblast<\/strong>\u00a0activity lead to collagen deposition, forming a\u00a0<strong>fibrous cap<\/strong>\u00a0over the plaque.<\/li>\n<li>Plaque can\u00a0<strong>calcify<\/strong>, making it more rigid, less elastic, and prone to\u00a0<strong>fissures<\/strong>\u00a0or rupture.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Progression:<\/strong>\n<ul>\n<li>Plaques grow larger,\u00a0<strong>narrowing the lumen<\/strong>.<\/li>\n<li>Leukocyte, platelet, and lipid accumulation worsen the obstruction.<\/li>\n<li>Turbulence from plaque causes further endothelial injury downstream, creating a\u00a0<strong>vicious cycle<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong> Consequences of Plaque Development:<\/strong><\/li>\n<\/ol>\n<ul>\n<li>Reduced blood flow causes\u00a0<strong>ischemia<\/strong>.<\/li>\n<li>Plates and thrombi can\u00a0<strong>embolize<\/strong>, leading to downstream blockages.<\/li>\n<li>Plaque rupture can trigger\u00a0<strong>acute events<\/strong>\u00a0like\u00a0<strong>heart attack<\/strong>\u00a0or\u00a0<strong>stroke<\/strong>.<\/li>\n<\/ul>\n<h1><strong>Risk Factors:<\/strong><\/h1>\n<table class=\"grid landscape\">\n<thead>\n<tr class=\"shaded\">\n<td><strong>Type<\/strong><\/td>\n<td><strong>Factors<\/strong><\/td>\n<td><strong>Description<\/strong><\/td>\n<\/tr>\n<\/thead>\n<tbody>\n<tr>\n<td><strong>Non-modifiable<\/strong><\/td>\n<td>Age, being male, genetic predisposition<\/td>\n<td>Can&#8217;t be changed; age-related plaque buildup common.<\/td>\n<\/tr>\n<tr>\n<td><strong>Modifiable<\/strong><\/td>\n<td>Obesity, smoking, sedentary lifestyle, poor diet, diabetes, hypertension, hormone therapy + smoking<\/td>\n<td>Lifestyle and health factors influencing plaque development.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<ul>\n<li><strong>Smoking:<\/strong>\n<ul>\n<li>Decreases\u00a0<strong>HDL (&#8220;good&#8221; cholesterol)<\/strong>, increases\u00a0<strong>LDL (&#8220;bad&#8221; cholesterol)<\/strong>.<\/li>\n<li>Promotes\u00a0<strong>vasoconstriction<\/strong>\u00a0and\u00a0<strong>platelet adhesion<\/strong>, increasing clot risk.<\/li>\n<li>Raises\u00a0<strong>heart rate<\/strong>\u00a0and\u00a0<strong>blood pressure<\/strong>.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Diabetes:<\/strong>\n<ul>\n<li>Elevates\u00a0<strong>glucose and lipid levels<\/strong>, damaging endothelium, promoting plaques.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Hypertension:<\/strong>\n<ul>\n<li>Causes\u00a0<strong>endothelial injury<\/strong>, accelerating plaque formation.<\/li>\n<\/ul>\n<\/li>\n<li><strong>Combination factors:<\/strong>\n<ul>\n<li>Use of\u00a0<strong>birth control pills<\/strong>\u00a0combined with\u00a0<strong>smoking<\/strong>\u00a0especially after age 35 greatly increases clotting risk.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<h1><strong>Summary:<\/strong><\/h1>\n<p><strong>Atherosclerosis<\/strong> involves fatty deposits causing vessel narrowing and turbulence, leading to progressive damage and risk of infarction.<\/p>\n<p><strong>Large arteries<\/strong> such as the <strong>aorta<\/strong> and <strong>coronary arteries<\/strong> are particularly vulnerable, and lifestyle factors heavily influence plaque development.<\/p>\n<p><strong>Key Concepts:<\/strong><\/p>\n<ul>\n<li><strong>LDL:<\/strong>\u00a0Delivers lipids but can promote plaque buildup if levels are high.<\/li>\n<li><strong>HDL:<\/strong>\u00a0Protects against atherosclerosis by cleaning up excess lipids.<\/li>\n<li>Managing lipid levels through diet, activity, and medications helps prevent or slow the progression of atherosclerosis.<\/li>\n<\/ul>\n<p><strong>Atherosclerosis<\/strong> begins with <strong>endothelial injury<\/strong> and progression involves <strong>lipid accumulation<\/strong>, <strong>inflammation,<\/strong> and <strong>plaque formation<\/strong>.<\/p>\n<p>Lifestyle factors like <strong>smoking, diet,<\/strong> and <strong>inactivity<\/strong> significantly influence disease progression, while medical interventions aim to prevent or remove plaques and reduce the risk of acute cardiovascular events.<\/p>\n<p>Surgical removal of plaques is possible, but <strong>prevention<\/strong> remains key.<\/p>\n","protected":false},"author":1370,"menu_order":25,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-5595","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":55,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5595","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":5,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5595\/revisions"}],"predecessor-version":[{"id":5600,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5595\/revisions\/5600"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/55"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/5595\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=5595"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=5595"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=5595"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=5595"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}