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Arten wie Meisen, Finken, Kleiber, Stieglitze usw. Diese starke Verminderung betrifft bei uns eigentlich alle Vogelarten.
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Atherosclerosis is a syndrome affecting arterial blood vessels. It is a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low density especially small particle lipoproteins plasma proteins that carry cholesterol and triglycerides without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins HDLsee apoA-1 Milano.
It is commonly referred to as a hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries. The atheromatous plaque is divided into three distinct components:. The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: Arteriosclerosis is a general term describing any hardening and loss of elasticity of medium or large arteries from the Greek ArterioAktion Thrombophlebitis, meaning arteryand sclerosismeaning 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.
Therefore, atherosclerosis is a form of arteriosclerosis. Atherosclerosis, though typically asymptomatic for decades, eventually produces two main problems: Firstthe atheromatous plaquesthough long compensated for by artery enlargement see IMTeventually lead to plaque ruptures and clots inside the artery lumen over the ruptures.
The clots heal and usually shrink but leave behind stenosis narrowing of the artery both locally and in smaller downstream branchesor worse, complete closure, and, therefore, Aktion Thrombophlebitis, an insufficient blood supply to the tissues and organ it feeds. SecondAktion Thrombophlebitis, if Aktion Thrombophlebitis compensating artery enlargement process is excessive, then a net aneurysm results.
These complications of advanced atherosclerosis are chronic, Aktion Thrombophlebitis, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures see vulnerable 100 Varizen Behandlungcausing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately 5 minutes.
This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of a coronary arterycausing myocardial infarction a heart attack. Even worse is the same process in an artery to the brain, commonly called stroke.
Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs, typically due to a combination of both stenosis and aneurysmal segments narrowed with clots. Since atherosclerosis Aktion Thrombophlebitis a body-wide process, similar events occur also in the arteries to the brain, intestines, kidneys, legs, etc. Yet, many infarctions involve only very small amounts of tissue and Aktion Thrombophlebitis termed clinically silentbecause the person having the infarction does not notice the problem, Aktion Thrombophlebitis, does not seek medical help or when they do, physicians do not recognize what has happened.
Atherosclerosis Aktion Thrombophlebitis from low-density lipoprotein molecules LDL becoming oxidized ldl-ox by free radicals, particularly oxygen free radicals ROS. Blood in arteries contains plenty of oxygen and is where atherosclerosis develops. Blood in veins contains little oxygen where atherosclerosis rarely develops. When oxidized LDL comes in contact with an artery wall, a series of reactions occur to repair the damage to the artery wall caused by oxidized LDL.
The LDL molecule is globular shaped with a hollow core to carry cholesterol throughout the body to generate brain tissues, Aktion Thrombophlebitis, vitamin D, and so on. Cholesterol does not dissolve in water. Aktion Thrombophlebitis can move in the bloodstream only by being transported by LDL. The body's immune system responds to the damage to the artery wall caused by oxidized LDL by sending specialized white blood cells macrophages and T-lymphocytes to absorb the oxidized-LDL forming specialized foam cells.
Unfortunately, these white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, Aktion Thrombophlebitis, depositing a greater amount of oxidized cholesterol into the artery wall.
This triggers more white blood cells, continuing the cycle. Krampfadern Behandlung Salben und Medikamente, the artery becomes inflamed. The cholesterol plaque causes the muscle cells to enlarge and form a hard cover over the affected area. This hard cover Aktion Thrombophlebitis what causes a narrowing of the artery, reduces the blood flow and increases blood pressure.
Some researchers believe that atherosclerosis may be caused by an infection of the vascular smooth muscle cells. Chickens, for example, develop atherosclerosis when infected with the Marek's disease herpesvirus.
Atherosclerosis typically begins in early adolescence, and is usually found in most major arteriesyet is asymptomatic and not detected by most diagnostic methods during life.
The stage immediately prior to actual atherosclerosis is known as subclinical atherosclerosis. The majority of the process leading to subclinical atherosclerosis can happen without our knowing it, especially given the large variety of risk factors. Atheroma in arm, or more often in leg arteries, which produces decreased blood flow is called peripheral Aktion ThrombophlebitisPostpartale Thrombophlebitis ist disease PAOD.
The relative geometry error within the illustration is common to many older illustrations, Aktion Thrombophlebitis, an error slowly being more commonly recognized within the last decade. Atherogenesis is the developmental process of atheromatous plaques. It is characterized by a remodeling of arteries involving the concomitant accumulation of fatty substances called plaques. One recent theory suggests that, for unknown reasons, leukocytesAktion Thrombophlebitis, such as monocytes or basophilsbegin to attack the endothelium of the artery lumen in cardiac muscle.
The ensuing inflammation leads to formation of atheromatous plaques in the arterial tunica intimaa region of the vessel wall located between the endothelium and the tunica media.
The bulk of these lesions is made of excess fat, collagenand elastin. At first, as the plaques grow, only wall thickening occurs without any narrowing, stenosis of the artery opening, called the lumen; stenosis is a late event, which may never occur and is often the result of repeated plaque rupture and healing responses, Aktion Thrombophlebitis, not just the atherosclerosis process by itself. The first step of atherogenesis is the development of so called " fatty streak "s, which are small sub-endothelial deposits of monocyte-derived macrophages.
The primary documented driver of this process is oxidized Lipoprotein particles within the wall, Aktion Thrombophlebitis the endothelial cells, though upper normal or elevated concentrations of blood glucose also plays a major role and not all factors are fully understood. Fatty streaks may appear and disappear. Low Density Lipoprotein particles in blood plasma, when they invade the endothelium and become oxidize Aktion Thrombophlebitis a risk for cardiovascular disease.
A complex set of biochemical reactions regulates Aktion Thrombophlebitis oxidation of LDL, chiefly stimulated by presence of enzymes, e. Lp-LpA2 and free radicals in Aktion Thrombophlebitis endothelium or blood vessel lining.
The initial damage to the blood vessel wall results in a "call for help," an inflammatory response. Monocytes a type of white blood cell enter the artery wall from the bloodstream, with platelets adhering to the area of insult.
This may be promoted by redox signaling induction of factors such as VCAM-1Aktion Thrombophlebitis, which recruit circulating monocytes. The monocytes differentiate macrophageswhich ingest oxidized LDLslowly turning into large "foam cells" — so-described because of their changed appearance resulting from the numerous internal cytoplasmic vesicles and resulting high lipid content.
Under the microscope, the lesion now appears as a fatty streak. Foam cells eventually die, and further propagate the inflammatory process. There is also smooth muscle proliferation and migration from tunica media to intima responding to cytokines secreted by damaged endothelial cells.
This would cause the formation of a fibrous capsule covering the fatty streak. Intracellular Aktion Thrombophlebitis form within vascular Aktion Thrombophlebitis muscle cells of the surrounding muscular layer, specifically in the muscle cells adjacent to the atheromas, Aktion Thrombophlebitis.
In time, as cells die, Aktion Thrombophlebitis, this leads to extracellular calcium deposits between the muscular wall and outer portion of the atheromatous plaques.
A similar form of an intramural calcification, Aktion Thrombophlebitis, presenting the picture of an early phase of arteriosclerosis, appears to be induced by a number of drugs that have an antiproliferative mechanism of action Rainer Liedtke Cholesterol is delivered into the vessel wall by cholesterol-containing low-density lipoprotein LDL particles. To attract and stimulate macrophages, the cholesterol must be released Aktion Thrombophlebitis the LDL particles and oxidized, a key step in the ongoing inflammatory process.
The process is worsened if there is insufficient high-density lipoprotein HDLthe lipoprotein particle that removes cholesterol from tissues and carries it back to the liver. The foam cells and platelets encourage the migration and proliferation of smooth muscle cells, which in turn ingest lipids, become replaced by collagen and transform into foam cells themselves.
A protective fibrous cap normally forms between the fatty deposits and the artery lining the intima. These capped fatty deposits now called 'atheromas' produce enzymes that cause the artery to enlarge over time, Aktion Thrombophlebitis. As long as the artery enlarges sufficiently to compensate for the extra thickness of the atheroma, then no narrowing Aktion Thrombophlebitis stenosis " of the opening "lumen" occurs, Aktion Thrombophlebitis.
The artery becomes expanded with an egg-shaped cross-section, still with a circular opening. If the enlargement is beyond proportion to the atheroma thickness, then an aneurysm is created. Although arteries are not typically studied Aktion Thrombophlebitis, two plaque types can be distinguished :. In effect, Aktion Thrombophlebitis, the muscular portion of the artery wall forms small Aktion Thrombophlebitis just large enough to hold the atheroma that are present.
The Aktion Thrombophlebitis portion of artery walls usually remain strong, even after they have remodeled to Aktion Thrombophlebitis for the atheromatous plaques. However, atheromas within the vessel wall are soft and fragile with little elasticity. Arteries constantly expand and contract with each heartbeat, i. In addition, the calcification deposits between the outer portion of the atheroma and the muscular wall, Aktion Thrombophlebitis, as they progress, lead to a loss of elasticity and stiffening of the artery as a whole.
The calcification deposits, after they have become sufficiently advanced, are partially visible on coronary artery computed tomography or electron beam tomography EBT as rings of increased radiographic density, forming halos around the outer edges of the atheromatous plaques, within the artery wall. These deposits demonstrate unequivocal evidence of the disease, relatively advanced, even though the lumen of the artery is often still normal by angiographic or intravascular ultrasound, Aktion Thrombophlebitis.
Although the disease process tends to be slowly progressive over decades, it usually remains asymptomatic until an atheroma obstructs the bloodstream in the artery. This is typically by rupture of an atheroma, clotting and fibrous organization of the clot within the lumen, covering the rupture but also producing stenosisor over time and Aktion Thrombophlebitis repeated ruptures, resulting in a persistent, usually localized stenosis. Repeated plaque Aktion Thrombophlebitis, ones not resulting in total lumen closure, combined with the clot patch over the rupture and healing response to stabilize the clot, Aktion Thrombophlebitis, is the process that produces most stenoses over time.
The stenotic areas tend to become more stable, despite increased flow velocities at these narrowings. Most major blood-flow-stopping events occur at large plaques, which, prior to their rupture, produced very little if any stenosis. Most severe clinical events do not occur at plaques that produce high-grade stenosis.
If the fibrous cap separating a soft atheroma from the bloodstream within the artery ruptures, tissue fragments are exposed and released, and blood enters the atheroma within the wall and sometimes results in a sudden expansion of the atheroma size. Tissue fragments are very clot-promoting, containing collagen and tissue factor ; they activate platelets and activate the system of coagulation.
The result is the formation of a thrombus blood clot overlying the atheroma, Aktion Thrombophlebitis, which obstructs blood flow acutely. With the obstruction of blood flow, downstream tissues are starved of oxygen and nutrients. If this is the myocardium heart muscleangina cardiac chest pain or myocardial infarction heart attack develops.
Areas of severe Aktion Thrombophlebitis, stenosisdetectable Aktion Thrombophlebitis angiography, and to a lesser extent " stress testing " have long been the focus of human diagnostic techniques for cardiovascular diseasein general. However, these methods focus on detecting only severe narrowingnot the underlying atherosclerosis disease. As demonstrated by human clinical studies, most severe events occur in locations with heavy plaque, yet little or no lumen narrowing present before debilitating events suddenly occur.
Plaque rupture can lead to artery lumen occlusion within seconds to minutes, and potential permanent Aktion Thrombophlebitis and sometimes sudden death. Plaques that have ruptured are called complicated plaques. The lipid matrix breaks through the thinning collagen gap and when the lipids come in contact with the blood, clotting occurs.
After rupture the platelet adhesion causes the clotting cascade to contact with the lipid pool causing a thrombus Aktion Thrombophlebitis form.
This thrombus will eventually grow and travel throughout the body, Aktion Thrombophlebitis.