Chapter 11: Blood vessels
While vascular pathologies are diverse in presentation they stem from two principle etiologies: stenosis i.e. narrowing of vessel lumina or weakening or vessel walls.
While arterial wall thickness gradually reduces as vessels become smaller the ratio of wall thickness to lumen diameter increases allowing smooth muscles to finely control blood flow and pressure. Because the vascular form and function correlate tightly with anatomy, their pathology correlates as well: atherosclerosis affects elastic muscular arteries; hypertension affects small muscular arteries and arterioles; and forms of vasculitis characteristically involves vessels of certain calibers.
All blood vessels are made of three layers or tunicas:
Intima: a single layer of endothelial cells that lines the lumin of the vessel ans is separated from the tunica media by the internal elastic lamina
Arteries have several well organized concentric layers while veins have much fewer cells that are poorly organized
The tunica media of highly elastic arteries contains significantly higher concentrations of elastin allowing for dynamic expanision and contraction during systole and dyastole
In muscular arteries, the tunica media consists predominately of smooth muscle, which is the main effector of regional blood flow and pressure by the autonomic nervous system.
While arterioles are less muscular they are the principle regulators of total peripheral resistance
Adventitia lies outside the media—from which it is separated by the external elasitc lamina—and consists of loose connective tissue, nerve fibers and arterioles that supply the outer portions of the media (vesa vasorum)
There are 3 subdivisions of arteries:
Elasitc arteries: large and include the 3 major branches of the aorta (innominate, subclavian, common carotid, and iliac arteries)
Muscular arteries: smaller branches of the aorta such as the coronary and renal arteries
Arterioles and small arteries: found within tissues and organs
Capillaries have no tunica media but are surrounded by a variable number of pericytes that have some smooth muscle function. The network of capillaries are most expansive in tissues with the highest demand for oxygen and nutrients i.e. the brain and heart. Capillaries flow directly in to postcapillary venules—the preferred site of vascular leakage and leukocyte exudation during most inflammatory reactions.
At the same levels of branching, veins contrast with arteries in terms of larger lumina and have thinner, less organized walls yet two thirds of all blood volume exists in venous circulation. They can be compressed, dilated, and are prone to tumor infiltrates and inflammation.
Lympatics are thin vessels with specialized endothelium responsible for return of interstitial fluid and inflammatory cells and are an important pathway for dissemination of disease as the can facilitate the transport of tumor cells and pathogenic microbes.
Some important congenital vascular disorders include:
Developmental or berry aneurysms: by definition, an vascular wall defect in the cerebral vessels that can be the cause of almost certainly fatal intracerebral hemorrhage.
Arteriovenous fistulas: direct connections between arteries and veins that bypass intervening capillary beds due to congenital defects, ruptured arterial aneurysms, of inflammatory necrosis of adjacent vessels. Pathology thereof includes: intracerebral hemorrhage or high-output cardiac failure (volume overload). Therapeutic fistulas can be created surgically to provide vascular access for chronic hemodialysis.
Fibromuscular dysplasia: idiopathic (but hereditary) hyperplasia and fibrosis of the intimal and medial layers of medium and large muscular arteries—namely renal, carotid, splanchnic, and vertebral—seen most frequently in young females. It can causes luminal stenosis and is an etiology of renovascular hypertension. Immediately adjacent segments of areas of stenosis have an attenuated tunica media giving a “string of beads” appearance.
Endothelial cells express diverse genetic profiles for specialized function in a given tissue e.g. fenestration in hepatic sinusoids and renal glomeruli. Systemically, endothelial cells are critical in thrombogeneis (or lack thereof); modulation of medial layer smooth muscle tone (e.g. angiotensin hormone); regulation of inflammation; and egress of fluids, ions, or proteins. Constitutive or inducible endothelial activation can be caused by cytokines, bacterial products, hemodynamic stress, glycation end-products, viruses, complement, and hypoxia. In response, they express adhesions molecules, cytoikines, growth factors, vasoactive signaling molecules, major histocompatibility complexes, anti- or pro-coagulant factors. Endothelial dysfunction typically describes sequelae that’s proinflammatory or prothrombogenic in nature.
The stereotypical response to vascular injury—associated with endothelial dysfunction—stimulates smooth muscle proliferation as well as their mobilization from uninjured areas and extracellular synthesis leading to intimal layer thickening. Neotintimal smooth muscle cells are proliferative, motile, and sensitive to signaling from cytokines, platelet derived growth factor, macrophages, thrombin, and complement.