Okumura CY, Nizet V: Subterfuge and sabotage: evasion of host innate defenses by invasive gram-positive bacterial pathogens, Annu Rev Microbiol 68:439, 2014. [A very good review of this complex area.]
Panchaud A, Stojanov M, Ammerdorffer A, et al: Emerging role of Zika v irus in adverse fetal and neonatal outcomes, Clin Microbiol Rev 29:659, 2016. [Review of emerging role of Zika virus in congenital brain defects.]
Safronetz D, Feldmann H, de Wit E: Birth and pathogenesis of rogue respiratory viruses, Annu Rev Pathol 10:449, 2015. [Introduces zoonotic respiratory review, with a good emphasis on pathogenesis.]
Sommer F, Backhed F: The gut microbiota—masters of host development and physiology, Nat Rev Microbiol 11:227, 2013. [An excellent introduction to intestinal microbiome and the role it plays in development of the immune response.]
Wlodarska M, Johnston JC, Gardy JL, et al: A microbiological revolution meets an ancient disease: improving the management of tuberculosis with genomics, Clin Microbiol Rev 28:523, 2015. [A good example of the important trend toward whole-bacterial genome sequencing in clinical diagnostics.] http://ebooksmedicine.net studentconsult.com
Epidemiology of Hypertension
Mechanisms of Essential Hypertension
Intimal Thickening: A Stereotypical Response to Vascular Injury
Epidemiology of Atherosclerosis
Clinicopathologic Consequences of
Varicose Veins of the Extremities
Varicosities of Other Sites
Vascular diseases are responsible for some of the most common and lethal conditions afflicting mankind. Although most clinically significant disorders involve arterial lesions, venous pathologies also can wreak havoc. Vascular disease develops through two principal mechanisms:
Narrowing or complete obstruction of vessel lumina, occurring either progressively (e.g., by atherosclerosis) or acutely (e.g., by thrombosis or embolism)
Weakening of vessel walls, causing dilation and/or rupture
We start with an overview of vascular structure and function, as background for the diseases of blood vessels discussed in the chapter.
Blood vessels are fundamentally all tubes composed of smooth muscle cells (SMCs) and extracellular matrix (ECM), with an inner luminal face covered by a continuous lining of endothelial cells (ECs). However, the relative amounts of SMCs and ECM, and the properties of the ECs, vary throughout the vasculature depending on unique functional needs (
Fig. 10.1 ). To accommodate pulsatile flow and higher blood pressures, arterial walls are thicker than veins and invested with several reinforcing layers of SMCs. As arteries narrow to arterioles, the ratio of wall thickness to lumen diameter increases to allow more precise regulation of intravascular pressure. Veins, on the other hand, are distensible thin-walled vessels with high capacitance. To facilitate maximal diffusion, capillaries are essentially single-cell linings of ECs lying on a basement membrane.
Since various vessels have unique structural features, it is not surprising that certain lesions characteristically involve only specific regions of the vasculature. For example, atherosclerosis occurs mainly in larger, muscular arteries, while hypertension affects small arterioles, and specific forms of vasculitis selectively involve vessels of only a certain caliber.
Vessel walls are organized into three concentric layers: intima, media, and adventitia (see