Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2
➤ Gửi thông báo lỗi ⚠️ Báo cáo tài liệu vi phạmNội dung chi tiết: Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2
Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2
SECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2PATHOGENESISAtherosclerosis remains the major cause ol death and premature disability' in developed societies. More over, current predictions estimate that by the year 2020 cardiovascular diseases, notably atherosclerosis, will become the leading global cause of total disease bur den. Although many Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2generalized or systemic risk factors predispose to its development, atherosclerosis affects various regions of the circulation preferentially and hasEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
distinct clinical manifestations that depend on the particular circulatory bed affected. Atherosclerosis ol the coronary arteries commonly causes myocSECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2vokes Strokes and transient cerebral ischemia. In the peripheral circulation, atherosclerosis causes intermittent claudication and gangrene and can jeopardize limb viability’. Involvement of the splanchnic circulation can cause mesenteric ischemia. Atherosclerosis can affect the kidneys either direc Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2tly (c.g., renal artery’ stenosis) or as a common site of alheroembolic disease (chap. 38).Even within a particular arterial bed. stenoses due to atheEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
rosclerosis tend to occur fiscally, typically in certain predisposed regions. In the coronary circulation, for example, the proximal left anterior desSECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2the proximal portions of the renal arteries and, in the extracranial circulation to the brain, the carotid bifurcation. Indeed, atherosclerotic lesions often form at branching points of arteries which are regions of disturbed blood flow. Not all manifestations of atherosclerosis result from stenotic Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2, occlusive disease. Ectasia and the development of aneurysmal disease, forexample, frequently occur in the aorta (Chap. 38). In addition to focal, flEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
ow limiting stenoses, nonoc elusive intimal atherosclerosis also occurs diffusely in affected arteries, as shown by intravascular ultrasound and postmSECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2ocs not occur in a smooth, linear fashion but discontinuously, with periods of relative quiescence punctuated by periods of rapid evolution. After a generally' prolonged “silent” period, atherosclerosis may’ become clinically’ manifest. The clinical expressions of atherosclerosis may be iiironii. as Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2 in the development of stable, effort induced angina pectoris or predictable and reproducible intermittent claudication. Alternatively. a dramatic acuEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
lc clinical event such as Ml, stroke, or sudden cardiac death may’ first herald the presence of atherosclerosis. Other indi viduals may never experienSECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2ISAn integrated view of experimental results in animals and studies of human atherosclerosis suggests that the “fatty streak” represents the initial lesion of atherosclerosis. These early lesions most often seem to arise from focal increases in the content of lipoproteins within regions of the intim Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2a. This accumulation of lipoprotein particles may not result simply from increased penne ability, or “leakiness.” of the overlying endothelium (Fig. 3Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2
0—1). Rather, the lipoproteins may collect in the intima of arteries because they bind to constituents of the extracellular matrix, increasing the resSECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2atheroma, from left to right. The upper panel shows a detail of the boxed area below. The endothelial monolayer overlying the intima contacts blood. Hypercholesterolemia promotes accumulation of LDL particles (tight spheres) in the intima. The lipoprotein particles often associate with constituents Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2of the extracellular matrix, notably proteoglycans. Sequestration within the intima separates lipoproteins from some plasma antioxidants and favors oxEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
idative modification. Such modified lipoprotein particles (darker spheres) may trigger a local inflammatory response that signals subsequent steps in SECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2nce adherent, some white blood cells migrate into the intima. The directed migration of leukocytes probably depends on chemoattractant factors, including modified lipoprotein particles themselves and chemoattractant cytokines (depicted by the smaller spheres), such as the Che mokine macrophage chemo Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2attractant protein-1 produced by vascular wall cells in response to modified lipoproteins. I eukocytes in the evolving fatty streak can divide and exhEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
ibit augmented expression of receptors for modified lipopro tans (scavenger receptors). These mononuclear phagocytes ingest lipids and become foam celSECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2ells migrate from the media (bottom of lower panel hairtine) through the internal clastic membrane (solid wavy line) and accumulate within the expanding intima, where they lay down extracellular matrix that forms the bulk of the advanced lesion (bottom panel, right side).Lipoproteins that accumulate Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2 in the extracellular space 341 of the intima of arteries often associate with glycosaminoglycans of the arterial extracellular matrix, an interactionEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
that may slow the egress of these lipid-rich particles from the intima. Lipoprotein particles in the extracellular space of the intima, particularly SECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2 of oxidized lipoproteins in athcrogencsis. Lipoproteins Er sequestered from plasma antioxidants in the extracellu- -o lar space of the intima become particularly susceptible =* to oxidative modification, giving rise to hydroper-oxides, lysophospholipids. oxysterols, and aldehydic 5 breakdown produc Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2ts ol fatty acids and phospholipids. g. Modifications of the apoprotein moicties may include breaks in the peptide backbone as well as derivatiza- 2 lEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
ion of certain ammo acid residues. Local production OÍ § hypochlorous acid by myeloperoxidase associated with o’ inflammatory cells within the plaque SECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2n poorly as cholesterol acceptors, a s finding that links oxidative stress with impaired reverse 3 cholesterol transport, which is one likely mechanism of 2. the antiatherogenic action ol 11DL (see later). Con- 2. siderable evidence supports the presence OÍ such 0X1- s dation products in atheroscler Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2otic lesions. A particular member ol the phospholipase family, lipoprotein- £ associated phospholipase A> (I.pPL A,), can genet 2 ate proinflam matoryEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
lipids, including lysophosphatidyl s choline-bearing oxidized lipid moielies from oxidized phospholipids found in oxidized low density lipopro reins SECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2 atherosclerotic lesions (Fig. 30-1). Thus, from its very inception, athcrogenesis involves ele ments of inflammation, a process that now provides a unifying theme in the pathogenesis oi this disease. T he inflammatory cell types typically found in the evolv ing atheroma include monocyte derived mac Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2rophages and lymphocytes. A number of adhesion molecules or receptors for leukocytes expressed on rhe surface of the arterial endothelial cell probablEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
y participate in the recruitment of leukocytes to the nascent atheroma. Constituents of oxidatively modified low-density lipoprotein can augment the eSECTION VDISORDERS OF THE VASCULATUREhttps: //k hoth u Vi e n .comCHAPTER 30THE PATHOGENESIS, PREVENTION, AND TREATMENT OF ATHEROSCLEROSISPeter LibbyP Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2ly with leukocyte recruitment, a key event in lesion formation.Disorders OÍ the Vasculature342 Laminar shear forces such xs those encountered in most regions of normal arteries also can suppress the expression of leukocyte adhesion molecules. Sites of predilection for atherosclerotic lesions (c.g., Ebook Harrison''s cardiovascular medicine (2nd edition): Part 2branch points) often have disturbed flow. Ordered, pulsatile laminar shear of normal blood flow augments the production of nitric oxide by endothelialEbook Harrison''s cardiovascular medicine (2nd edition): Part 2
cells. This molecule. in addition to Its vasodilator properties, can act at the low levels constitutively produced by arterial endothelium xs a localGọi ngay
Chat zalo
Facebook