Fibrin Forms A Stable Clot Through Activation By' title='Fibrin Forms A Stable Clot Through Activation By' />Atherosclerosis Wikipedia.Atherosclerosis also known as arteriosclerotic vascular disease or ASVD is a specific form of arteriosclerosis in which an artery wall thickens as a result of invasion and accumulation of white blood cells macrophages and foam cells and proliferation of intimal smooth muscle cell creating an atheromatous fibrofatty plaque.The accumulation of the white blood cells is termed fatty streaks early on because of the appearance being similar to that of marbled steak.These accumulations contain both living, active white blood cells producing inflammation and remnants of dead cells, including cholesterol and triglycerides.Chapter 1 HISTOLOGY METHOD AND MICROSCOPY A NATURE OF HISTOLOGY Medical histology applies microscopy to the human body, seeking to discover the nature of its smaller.Start studying Ch.Learn vocabulary, terms, and more with flashcards, games, and other study tools.Fibrin Forms A Stable Clot Through Activation By' title='Fibrin Forms A Stable Clot Through Activation By' />The remnants eventually include calcium and other crystallized materials within the outermost and oldest plaque.The fatty streaks reduce the elasticity of the artery walls.However, they do not affect blood flow for decades because the artery muscular wall enlarges at the locations of plaque.The wall stiffening may eventually increase pulse pressure widened pulse pressure is one possible result of advanced disease within the major arteries.Atherosclerosis is therefore a syndrome affecting arterial blood vessels due to a chronic inflammatory response of white blood cells in the walls of arteries.This is promoted by low density lipoproteins LDL, plasma proteins that carry cholesterol and triglycerides without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins HDL.Two pathways lead to the formation of a fibrin clot the intrinsic and extrinsic pathway.Although they are initiated by distinct mechanisms, the two converge on a.Issuu is a digital publishing platform that makes it simple to publish magazines, catalogs, newspapers, books, and more online.Easily share your publications and get.It is commonly referred to as a hardening or furring of the arteries.It is caused by the formation of multiple atheromatous plaques within the arteries.One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction a heart attack.The same process in an artery to the brain is commonly called stroke.Another common scenario in advanced disease is claudication from insufficient blood supply to the legs.Atherosclerosis affects mostly larger, high pressure vessels such as the coronary, renal, femoral, cerebral, and carotid arteries.DefinitionseditThe following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused arteriosclerosis, arteriolosclerosis, and atherosclerosis.Arteriosclerosis is a general term describing any hardening and loss of elasticity of medium or large arteries from Greek artria, meaning artery, and sklerosis, meaning hardening arteriolosclerosis is any hardening and loss of elasticity of arterioles small arteries atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque.The term atherogenic is used for substances or processes that cause atherosclerosis.Signs and symptomseditAtherosclerosis is asymptomatic for decades because the arteries enlarge at all plaque locations, thus there is no effect on blood flow.Even most plaque ruptures do not produce symptoms until enough narrowing or closure of an artery, due to clots, occurs.Signs and symptoms only occur after severe narrowing or closure impedes blood flow to different organs enough to induce symptoms.Most of the time, patients realize that they have the disease only when they experience other cardiovascular disorders such as stroke or heart attack.These symptoms, however, still vary depending on which artery or organ is affected.Typically, atherosclerosis begins in childhood, as a thin layer of white yellowish streaks with the inner layers of the artery walls an accumulation of white blood cells, mostly monocytesmacrophages and progresses from there.Clinically, given enlargement of the arteries for decades, symptomatic atherosclerosis is typically associated with men in their 4.Sub clinically, the disease begins to appear in childhood, and rarely is already present at birth.Noticeable signs can begin developing at puberty.Though symptoms are rarely exhibited in children, early screening of children for cardiovascular diseases could be beneficial to both the child and hisher relatives.While coronary artery disease is more prevalent in men than women, atherosclerosis of the cerebral arteries and strokes equally affect both sexes.Marked narrowing in the coronary arteries, which are responsible for bringing oxygenated blood to the heart, can produce symptoms such as the chest pain of angina and shortness of breath, sweating, nausea, dizziness or light headedness, breathlessness or palpitations.Abnormal heart rhythms called arrhythmias the heart is either beating too slow or too fast are another consequence of ischemia.Carotid arteries supply blood to the brain and neck.Marked narrowing of the carotid arteries can present with symptoms such as a feeling of weakness, not being able to think straight, difficulty speaking, becoming dizzy and difficulty in walking or standing up straight, blurred vision, numbness of the face, arms, and legs, severe headache and losing consciousness.These symptoms are also related to stroke death of brain cells.Stroke is caused by marked narrowing or closure of arteries going to the brain lack of adequate blood supply leads to the death of the cells of the affected tissue.Peripheral arteries, which supply blood to the legs, arms, and pelvis, also experience marked narrowing due to plaque rupture and clots.Symptoms for the marked narrowing are numbness within the arms or legs, as well as pain.Another significant location for the plaque formation is the renal arteries, which supply blood to the kidneys.Plaque occurrence and accumulation leads to decreased kidney blood flow and chronic kidney disease, which, like all other areas, are typically asymptomatic until late stages.According to United States data for 2.Cardiac stress testing, traditionally the most commonly performed non invasive testing method for blood flow limitations, in general, detects only lumen narrowing of 7.Case studies have included autopsies of U.S. soldiers killed in World War II and the Korean War.A much cited report involved autopsies of 3.U. S. soldiers killed in Korea.Although the average age of the men was 2.Other studies done of soldiers in the Vietnam War showed similar results, although often worse than the ones from the earlier wars.Theories include high rates of tobacco use and in the case of the Vietnam soldiers the advent of processed foods after World War II.Risk factorsedit.Atherosclerosis and lipoproteins.The atherosclerotic process is not fully understood.Atherosclerosis is initiated by inflammatory processes in the endothelial cells of the vessel wall associated with retained low density lipoprotein LDL particles.This retention may be a cause, an effect, or both, of the underlying inflammatory process.The presence of the plaque induces the muscle cells of the blood vessel to stretch, compensating for the additional bulk, and the endothelial lining thickens, increasing the separation between the plaque and lumen.This somewhat offsets the narrowing caused by the growth of the plaque, but it causes the wall to stiffen and become less compliant to stretching with each heart beat.ModifiableeditNonmodifiableeditLesser or uncertaineditDietaryeditThe relation between dietary fat and atherosclerosis is controversial.Writing in Science, Gary Taubes detailed that political considerations played into the recommendations of government bodies.The USDA, in its food pyramid, promotes a diet of about 6.The American Heart Association, the American Diabetes Association and the National Cholesterol Education Program make similar recommendations.In contrast, Prof Walter Willett Harvard School of Public Health, PI of the second Nurses Health Study recommends much higher levels of fat, especially of monounsaturated and polyunsaturated fat.These differing views reach a consensus, though, against consumption of trans fats.The role of dietary oxidized fatslipid peroxidation rancid fats in humans is not clear.Laboratory animals fed rancid fats develop atherosclerosis.Rats fed DHA containing oils experienced marked disruptions to their antioxidant systems, and accumulated significant amounts of phospholipidhydroperoxide in their blood, livers and kidneys.Rabbits fed atherogenic diets containing various oils were found to undergo the greatest amount of oxidative susceptibility of LDL via polyunsaturated oils.Dr. Malcolm Kendrick Scottish Doctor, author, speaker, sceptic.September 2. 01. 7Wipe your mind clear of all previous ideas about CVD.About as easy as standing in the corner and not thinking about a tiger.In reality, once you have read about, and talked about, and researched, and thought about anything, patterns are created in your mind.Familiar landscapes develop, and well worn pathways become the comfortable and easy routes to travel down.Say what you like about Ancel Keys and I had better not, for I would end up swearing a lot, he created the tightly patrolled mental box for everyone.Diet and cholesterol and cardiovascular disease.These are the great beacons that mark out, the map of the mind, where all thinking and discussion must take place.They illuminate all, and beyond them is darkness.Now, blow out the beacons.Move out into darkness.We shall create a new landscape of thought.We have control of the vertical, and the horizontal, you are entering the Outer Limits.I suspect some people may not get that reference.We are breaking free of the box. Driver Per Tomtom Go 910 Hack . In fact, there is no box, it no longer exists.In the distance, there is a glimmer of light it is our first fact.At least we hope it is a fact.We approach the glittering light and scrape way the grime that has been obscuring it for many years, to revealAtherosclerotic plaques only develop in larger arteries.Quite close to it, almost hidden away, lies another fact.Atherosclerotic plaques never develop in veins.There are two exceptions to the second fact well, there are more, but these are the most obvious.First, if you take a vein, and use it to create a coronary artery bypass graft, it will develop atherosclerosis very rapidly.Secondly, if you create an arteriovenous fistula AV fistula fusing an artery and vein together for dialysis patients, the venous section will develop atherosclerotic plaques.Setting aside these exceptions, these two facts were as close to inarguable as I have been able to find.Inevitably, they lead to my first question.Why do plaques develop in arteries, and not in veins Right now, I can see you doing what everyone does, searching for a simple answer, with thoughts such as There is less oxygen in veins, and oxygenation is damaging to arterial walls.The pressure is less in veins.The LDL level is lower in veins its not, but I have heard a lot of people say thisArteries and veins have a different structure they do not.And so on, and so forth.Isnt the search for a quick and simple answer fun After exploring almost every avenue that I believed could possibly be involved in CVD, I found myself returning more and more often to the difference in blood pressure in veins and arteries as the place where the answers were most likely to be found.However, I knew pressure, by itself, is not going to cause anything, unless you succeed in bursting an artery, or bursting the lining of the artery.I mean, this can be done.You can develop an aneurysm thinned and ballooned area in an artery, which can then rupture usually with catastrophic consequences.But before that, what can pressure do Force things carried within the artery into the artery wall behind No, that does not make sense.For that would mean everything carried in the bloodstream would simply be blasted into all artery walls, everywhere.The smallest molecules would go first, molecules such H2.Does this happen.No, of course not.Our arteries, and the endothelial cells that line our arteries and veins, are not leaky.In short, differences in pressure cannot provide any sort of an explanation.However, there is a law of fluid dynamics which says words to the effect if the pressure in a tube is higher, the velocity of the fluid flowing through a tube will also be higher.Which means that blood is travelling far faster in an artery than a vein.A veritable white water maelstrom, compared to a meandering river as it approaches the sea.Thus, it is easy to imagine that anything lining an artery is going to be exposed to far greater forces than anything lining a vein.These forces, which I shall call biomechanical stresses, will be particularly intense in certain places.For example, where arteries branch bifurcate e.Another place of extreme biomechanical stress is within the coronary arteries.These arteries are exposed to a unique stress, in that they are compressed with great force when the heart contracts.Some have likened this to stomping on a hose every second.Indeed, blood cannot flow in coronary arteries during systole ventricular contraction because they are squeezed shut.In general, if you look at where atherosclerotic plaques develop, you find that they most often occur at maximum biomechanical stress.Where carotid arteries main arteries supplying blood to the brain branch from the aorta, and also where other arteries branch from the aorta, and within the coronary arteries.It seems, therefore, that biomechanical stress is required for plaques to develop.This is not the same as high blood pressure, but it is closely associated with high blood pressure.In truth, this idea is not in any way contentious.This is a highly jargon filled section from a paper called Biomechanics of Atherosclerotic Coronary Plaque Site, Stability and In Vivo Elasticity Modelling.Although the coronary and peripheral systems in their entirety are exposed to the same atherogenic cells and molecules in the plasma, atherosclerotic lesions form at specific regions of the arterial tree.Such lesions appear in the vicinity of branch points, the outer wall of bifurcations and the inner wall of curves.Pathologic studies, have shown that healed plaque ruptures are predominantly in the proximal portions of the left anterior descending LAD, right coronary RCA, left circumflex LCx and left main LM arteries.Investigations over the last decade have elucidated both fluid mechanical and most recently structural biomechanical factors that mediated the site of plaque formation.Which is all fine and sensible.However, this very same paper states the following Plaque formation is now recognized as an inflammatory process triggered by high levels of serum LDL that enter the coronary wall, encounter oxygen reactive species, and become oxidized.The oxidization, in turn, stimulates the recruitment of monocytes that convert to macrophages to phagocytize oxidized LDLs.This forms a necrotic core with recruitment of smooth muscle cells from the media to seal over the fatty core.That is the official party line as to how CVD starts, and develops.But if you believe that, you immediately face a conundrum.How can you reconcile the hypothesis that raised LDL entering the artery wall initiates plaque development, with the observation that atherosclerotic lesions form at specific regions of the arterial tree It is surely one, or the other, but it cannot be both.Sorry, but at this point I need to take you back into the landscape of raised LDL and CVD.You may think, in fact you probably are already thinking Well, biomechanical stress damages the endothelial cells, allowing LDL to enter.Now, that could be true.However, if that is true, then you have if you believe in the cholesterol hypothesis, just made a move that will result in checkmate against you.The argument goes like this If LDL can only leak into the artery wall at an area where the endothelial layer is damaged, and this is where plaques develop, this means it cannot leak through in areas where the endothelium is not damaged.Ergo, the first step in the development of plaques cannot be LDL leaking into the artery wall past the endothelium, it is damage to the endothelium.Ergo, a raised LDL level is not the primary cause of CVD.Checkmate. You dont like that logic If you prefer a few more facts, using a different approach.If you think LDL is capable of, simply, transporting itself past the endothelium, then you need to define a mechanism.Is it simply osmotic pressure, with LDL travelling down a concentration gradient from the bloodstream into the artery wall Is it actively transported through endothelial cells Does it leak between the endothelial cells These are the mechanisms that I have seen most commonly proposed although they are often presented with so much surrounding jargon that it is almost impossible to work out what is being said.
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