Blood Vessels Flashcards
(53 cards)
Blood vessels wall constituents
The basic constituents of the walls of blood vessels are endothelial cells and smooth muscle cells, admixed with a variety of extracellular matrix, including elastin, collagen, and glycosaminoglycans
Intimal components
The intima normally consists of a single layer of endo- thelial cells sitting on a basement membrane underlaid by a thin layer of extracellular matrix; the intima is demarcated from the media by the internal elastic lamina.
Media components
The media of vessels on the arterial side of the circulation varies in structure according to functional demands.
• Arteries have several well-organized concentric
layers of smooth muscle cells, while the smooth muscle cells of veins are arranged in a more haphaz- ard fashion.
Elastic arteries (aorta)- high elastin content
Muscular arteries & arterioles- circumferentially oriented smooth muscle
Adventitia components
The adventitia lies external to the media and in many arteries is separated from the media by a well-de ned external elastic lamina. The adventitia consists of loose connective tissue containing nerve bers and the vasa vasorum (literally “vessels of the vessels”), small arterioles that are responsible for supplying the outer portion of the media of large arteries with oxygen and nutrients.
Arterioles main function
Arterioles are the principal points of physiologic resistance to blood ow.
Intimal thickening
Stereotyped response to endothelial injury
Vascular injury—associated with endothelial cell dys- function or loss—stimulates smooth muscle cell recruit- ment and proliferation and associated matrix synthesis; the result is intimal thickening. Healing of injured vessels is analogous to the healing process that occurs in other damaged tissues
Hypertensive vascular disease
Systemic and local tissue blood pressures must be maintained within a narrow range to prevent untoward consequences.
high blood pressure (hyperten- sion) can cause end-organ damage and is one of the major risk factors for atherosclerosis
Hypotension
Low blood pressure (hypotension) results in inadequate organ perfusion and can lead to tissue dysfunction or death.
Arteriosclerosis
Arteriosclerosis literally means “hardening of the arteries”; it is a generic term for arterial wall thickening and loss of elasticity. There are three general patterns, with different clinical and pathologic consequences:
Arteriolosclerosis affects small arteries and arterioles, and may cause downstream ischemic injury. The two ana- tomic variants, hyaline and hyperplastic, are discussed earlier in relation to hypertension.
• Mönckeberg medial sclerosis is characterized by calci ca- tion of the walls of muscular arteries, typically involv- ing the internal elastic membrane. Persons older than age 50 are most commonly affected. The calcifcations
do not encroach on the vessel lumen and are usually not
clinically signi cant.
• Atherosclerosis, from Greek root words for “gruel” and
“hardening,” is the most frequent and clinically impor- tant pattern and is discussed here.
Atherosclerosis
Atherosclerosis underlies the pathogenesis of coronary, cerebral and peripheral vascular disease, and causes more morbidity and mortality (roughly half of all deaths) in the Western world than any other disorder.
Atherosclerosis pathogenesis 7
Endothelial injury and dysfunction, causing (among other things) increased vascular permeability, leukocyte adhesion, and thrombosis
• Accumulation of lipoproteins (mainly LDL and its oxi- dized forms) in the vessel wall
• Monocyte adhesion to the endothelium, followed by migra- tion into the intima and transformation into macrophages and foam cells
• Platelet adhesion
• Factor release from activated platelets, macrophages, and
vascular wall cells, inducing smooth muscle cell recruit- ment, either from the media or from circulating precursors
• Smooth muscle cell proliferation, extracellular matrix produc- tion, and recruitment of T cells.
• Lipid accumulation both extracellularly and within cells (macrophages and smooth muscle cell)
Atherosclerotic plaque components 3
Atherosclerotic plaques have three principal com- ponents: (1) smooth muscle cells, macrophages, and T cells; (2) extracellular matrix, including collagen, elastic bers, and proteoglycans; and (3) intracellular and extra- cellular lipid
Atherosclerosis complications 4
Rupture, ulceration, or erosion of the surface of athero- matous plaques exposes highly thrombogenic substances and leads to thrombosis, which may partially or completely occlude the vessel lumen (Fig. 11-15). If the patient survives, the clot may become organized and incorporated into the growing plaque.
• Hemorrhage into a plaque. Rupture of the overlying brous cap, or of the thin-walled vessels in the areas of neovascu- larization, can cause intraplaque hemorrhage; a contained hematoma may expand the plaque or induce plaque rupture.
• Atheroembolism. Plaque rupture can discharge atheroscle- rotic debris into the bloodstream, producing microemboli. • Aneurysm formation. Atherosclerosis-induced pressure or
ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness and potential rupture.
Atherosclerosis consequences
Symptomatic atherosclerotic disease most often involves the arteries supplying the heart, brain, kidneys, and lower extremities. Myocardial infarction (heart attack), cerebral infarction (stroke), aortic aneurysms, and peripheral vascular disease (gangrene of the legs) are the major consequences of atherosclerosis.
Aorta- media mostly composed of
Elastic fibers
Aorta- media can be stained with
Elastic stains - not H&E
The elastic stains color the aorta in black - can count the layers of elastic tissue
Capillaries structure
1 or 2 layers of ENDOTHELITAL cells. * surrounded by connective tissue * containing collagen
NO elastic fibers, NO smooth muscle cells
Veins wall
Less organized, less stratifies, low resistance
MUSCLE & ELASTIC FIBERS + collagen + ECM
large veins have more muscular tissue
Ischemic diseases in the body cause
Vessels pathology, diseases
Dilation of a vessel can leas to
Rupture, hemorrhage
Vena cava
Smooth muscle cells - stained red
Dispersed in collagen - stains green
NO ELASTIC LAMINA ??
Vascular pathology is responsible for
More morbidity & mortality than any other human disease
Mechanism of vascular disease- narrowing
When in arteries - reduction of blood supply
When in veins- blood stasis
Mechanism of vascular disease
Dilation - weakening of the vessel wall
LOSS OF MUSCULAR & ELASTIC COMPONENTS
