Aktion Thrombophlebitis

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JavaScript is currently disabled, Aktion Thrombophlebitis, this site works much better if you enable JavaScript in your browser. Click here to sign up. For the academic login, please select your country in the dropdown list. You will be redirected to verify your credentials. Glycosaminoglycans Veins Varicose veins Thrombophlebitis.

I have read the Karger Terms and Conditions and agree. If you would like to redeem your KAB credit, please log in. The aim of the study was to examine the content and molecular differentiation of glycosaminoglycans GAGs in the wall of varicose veins.

The studied material consisted of normal, varicose veins and varicose veins complicated by thrombophlebitis collected during operations on 26 patients. Furthermore, the increased quantitative ratio between sulphated and nonsulphated GAGs was demonstrated, Aktion Thrombophlebitis. The results indicate an evident extracellular matrix Aktion Thrombophlebitis in the wall of varicose veins particularly those complicated by thrombophlebitis, that is characterised by alterations in the content and molecular differentiation of GAGs.

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May 02, Issue release date: January — February Number of Print Pages: Abstract The aim of the study was to examine the content and molecular differentiation of glycosaminoglycans GAGs in the wall of varicose veins. Connective tissue in varicose veins.

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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 HDLAktion Thrombophlebitis, see apoA-1 Milano.

It is commonly referred to as Aktion Thrombophlebitis hardening or furring of the arteries. It is caused by the formation of multiple plaques within the arteries. The atheromatous plaque is divided into Aktion Thrombophlebitis 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 Arteriomeaning arteryand sclerosismeaning hardening ; arteriolosclerosis is any hardening and loss of elasticity Aktion Thrombophlebitis arterioles small arteries ; atherosclerosis is a hardening of an artery specifically due to an atheromatous Aktion Thrombophlebitis. Therefore, atherosclerosis is a form of arteriosclerosis, Aktion Thrombophlebitis.

Atherosclerosis, though typically asymptomatic for decades, Aktion Thrombophlebitis, 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 Aktion Thrombophlebitis narrowing of the artery both locally and Aktion Thrombophlebitis smaller downstream branchesor worse, complete closure, and, therefore, an insufficient blood Aktion Thrombophlebitis to the tissues and organ it feeds.

Secondif the compensating Aktion Thrombophlebitis enlargement process is excessive, then a net aneurysm results. These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative.

Most commonly, Aktion Thrombophlebitis, soft plaque suddenly ruptures see vulnerable plaquecausing 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, Aktion Thrombophlebitis. 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 is a body-wide process, similar events occur also in the arteries to the brain, intestines, kidneys, legs, Aktion Thrombophlebitis, etc. Yet, many infarctions involve only very small amounts of tissue and are termed clinically silentbecause the person having the infarction does not notice the problem, does not seek medical help or when they do, physicians do not recognize Aktion Thrombophlebitis has happened.

Atherosclerosis develops 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, Aktion Thrombophlebitis.

The LDL molecule is globular shaped with a Aktion Thrombophlebitis core to carry cholesterol throughout the body to generate brain tissues, vitamin D, and so on, Aktion Thrombophlebitis.

Cholesterol does not dissolve in water, Aktion Thrombophlebitis. Cholesterol 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, Aktion Thrombophlebitis. Unfortunately, these white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, depositing a greater amount of oxidized cholesterol into the artery wall.

This triggers more white blood cells, continuing the cycle. Eventually, Aktion Thrombophlebitis, 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 is what causes a narrowing of the artery, Aktion Thrombophlebitis, 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, Aktion Thrombophlebitis, for example, Aktion Thrombophlebitis, 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 Aktion Thrombophlebitis during life.

Aktion Thrombophlebitis stage immediately Aktion Thrombophlebitis 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 artery occlusive disease PAOD. The relative geometry error within the illustration is common to Aktion Thrombophlebitis older illustrations, 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, leukocytessuch 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, Aktion Thrombophlebitis, 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, Aktion Thrombophlebitis, which are small sub-endothelial deposits of monocyte-derived macrophages. The primary documented driver of this process is oxidized Lipoprotein particles within the wall, beneath 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 creates a risk for cardiovascular disease. A complex set of biochemical reactions regulates the oxidation of LDL, chiefly stimulated by presence of enzymes, e. Lp-LpA2 and free radicals in the endothelium or blood vessel lining, Aktion Thrombophlebitis.

Aktion Thrombophlebitis 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-1which 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 Aktion Thrombophlebitis high lipid content.

Under the microscope, Aktion Thrombophlebitis, the lesion now appears as a fatty streak. Foam cells eventually die, and further propagate the inflammatory process, Aktion Thrombophlebitis.

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 microcalcifications form within vascular smooth muscle cells of the surrounding muscular layer, specifically in the muscle cells adjacent Aktion Thrombophlebitis the atheromas.

In time, as cells die, 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, Aktion Thrombophlebitis 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 from 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, Aktion Thrombophlebitis. 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.

As long as the artery enlarges sufficiently to compensate for the extra thickness of the atheroma, then no narrowing " stenosis " of the opening "lumen" occurs. 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, Aktion Thrombophlebitis. Although arteries are not typically studied microscopically, two plaque types can be distinguished [1]:. In effect, the muscular portion of the artery wall forms small aneurysms just large enough to hold the atheroma that are present. The muscular portion of artery walls usually remain strong, Aktion Thrombophlebitis, even after they have remodeled to compensate for the atheromatous plaques.

However, Aktion Thrombophlebitis, 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 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 Aktion Thrombophlebitis 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, Aktion Thrombophlebitis, relatively advanced, Aktion Thrombophlebitis, even though the lumen of the artery is often Aktion Thrombophlebitis normal by angiographic or intravascular ultrasound, Aktion Thrombophlebitis.

Although the disease process tends to be slowly progressive trombotsid von Krampfadern decades, it usually remains asymptomatic until an atheroma obstructs the bloodstream in the Aktion Thrombophlebitis. This is typically by rupture of an Aktion Thrombophlebitis, clotting and fibrous organization of the clot within the lumen, covering the rupture but also producing stenosisor over time and after repeated ruptures, Aktion Thrombophlebitis in a persistent, usually localized stenosis.

Repeated plaque ruptures, ones not resulting in total lumen closure, combined with the clot patch over the rupture and healing response to stabilize the clot, 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, Aktion Thrombophlebitis, 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 Aktion Thrombophlebitis thrombus blood clot overlying the atheroma, which obstructs blood flow acutely. With the obstruction of blood flow, Aktion Thrombophlebitis, downstream tissues are starved of oxygen and nutrients, Aktion Thrombophlebitis.

If this is the myocardium heart muscleangina cardiac chest pain or myocardial infarction heart attack develops. Areas of severe narrowing, stenosisdetectable by angiography, and to a lesser extent " stress testing " have long been the focus of human diagnostic techniques for cardiovascular diseasein general, Aktion Thrombophlebitis.

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, Aktion Thrombophlebitis, yet little or no lumen narrowing present before debilitating events suddenly occur, Aktion Thrombophlebitis. Plaque rupture can lead to artery lumen occlusion within seconds to minutes, and potential permanent debility 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 to form. This thrombus will eventually grow and travel throughout the body.

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