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How Atherosclerosis Changes a Functional Circulatory System as Seen Through the Research of Histology

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The histopathology of atherosclerosis: Changes in functional histology and its repercussions

Functional histology of the healthy tissue

As explained by Young et al. (2014, p. 144), the circulatory system of the human body has two components: the blood vascular system and the lymphovascular system. In the blood vascular system (or, the blood circulatory system), the heart and its contractions pump blood into a network of blood vessels. This network is divided into the arterial and venous systems (Young et al. 2014, p. 144). The arterial system is responsible for providing gas (oxygen) and nutrients to the tissues (Damjanov et al. 2011, p.1) and taking blood to the capillaries (Young et al. 2014, p. 148), while the venous system is responsible for removing carbon dioxide and waste products that result from cellular respiration (Damjanov et al. 2011, p. 1) and returning blood from the capillaries to the heart (Young et al. 2014, p. 144). The blood circulatory system has three types of blood vessels: arteries, veins, and capillaries (Damjanov et al. 2011, p. 1).

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These various blood vessels of the circulatory system share a few structural components (Young et al. 2014, p. 144). The basic blood vessel model is characterized by the presence of three layers: the tunica intima, the tunica media, and the tunica adventitia (Figure 1) (Damjanov et al. 2011, p. 1). The tunica intima is the innermost layer (Young et al. 2014, p. 144). It is composed of endothelial cells (simple squamous epithelial cells) that make up the endothelium that lines all blood vessels (Figure 2) (Young et al. 2014, p. 144). The endocardium layer of the heart directly transitions to become the endothelium in blood vessels (Damjanov et al. 2011, p. 1). A basement membrane and collagenous tissue, known as the subendothelial layer (Young et al. 2014, p. 149) typically underlie the tunica intima (Young et al. 2014, p. 144). This subendothelial layer often has many elastin fibers and sheets in addition to the collagen (Young et al. 2014, p. 149). Fibroblasts and myointimal cells, similar in structure to smooth muscle cells, may also be present and contribute to the extracellular matrix (Young et al. 2014, p. 149). The next middle layer, the tunica media, is thicker than the tunica intima and is composed of elastin, smooth muscle, and collagen (Figure 3) (Young et al. 2014, p. 149). The outermost layer is the tunica adventitia, and it functions in providing support (Figure 4) (Young et al. 2014, p. 144). Also present in the adventitia are vasa vasorum, which are blood vessels present in the outer layers of larger arteries, such as the aorta, in order to provide the periphery of the vessel with gas and nutrient exchange, since these layers may be too far from the lumen to perform these functions on their own (Young et al. 2014, p. 149). Smooth muscle, elastin, and collagen are some of the elements that compose the walls of all blood vessels, and in particular, the various types of arteries (Stevens et al. 2002, p. 86).

As described by Young et al. (2014, p. 148), the arterial system has three types of blood vessels, which are the elastic arteries, the muscular arteries, and the arterioles. Elastic arteries are the primary distributive vessels. Examples include the aorta and the innominate, common carotid, subclavian, and larger pulmonary arteries. Muscular arteries are the primary distributive extensions of the arterial tree. Examples include the radial, femoral, coronary, and cerebral arteries. Arterioles are the ends of the arterial tree and supply blood to the capillary bed (Young et al. 2014, p. 148).

These three types of arteries gradually transition into one another and adhere to the common pattern of tunica intima, media, and adventitia, but with a few variations to aid their specialized functions (Young et al. 2014, p. 148). Arteries have abundant elastin and have a thicker smooth muscle layer when compared to the diameter of their lumen. These elastic tissue components allow arteries to expand and recoil, which allows the body to keep a relatively constant pressure in between heart beats (Young et al. 2014, p. 148). Changing the diameter of the blood vessels, known as vasoconstriction (reducing the diameter) or vasodilation (increasing the diameter), regulates the flow of blood throughout the body (Young et al. 2014, p. 148). This constriction or dilation in the vessel wall is controlled by the sympathetic nervous system and the hormones from the adrenal medulla, which coordinate the smooth muscle tissue in the vessel walls (Young et al. 2014, p. 148). A typical, functioning artery is comprised of five parts (from interior to exterior): the endothelium, the tunica intima, the internal elastic lamina, the tunica media, and the tunica adventitia (Figure 5) (Stevens et al. 2002, p. 87). The slim tunica intima is made up of the endothelium that borders the inside of the artery and the internal elastic lamina (Stevens et al. 2002, p. 148). It is also made up of fibroelastic, loose connective tissue. Myointimal cells may be present in this layer, but are sometimes hard to find (Stevens et al. 2002, p. 87). The tunica media is a smooth muscle layer that also includes a few elastic fibers (Stevens et al. 2002, p. 87). As blood vessels become smaller, the elastic tissue component diminishes, allowing for the smooth muscle tissue to become more notable (Young et al. 2014, p. 148).

According to Damjanov et al. (2011, p. 1), the large, elastic arteries, including the aorta, are characterized by the presence of fenestrated elastic bundles, which are interspersed with collagen fibers and some smooth muscle in the tunica media. Muscular arteries, smaller than elastic arteries, are characterized by the prevalent smooth muscle in the tunica media. They are also characterized by the internal elastic lamina, located to the outer side of the tunica intima, and the external elastic lamina, towards the outside of the tunica media. Muscular arteries transition into arterioles, which have an endothelial cell and smooth muscle cell layer, which develop into capillaries that are continuous with venules (Damjanov et al. 2011, p. 1).

Atherosclerosis

“Arteriosclerosis” refers to a broad category of diseases that share a similar characteristic: the walls of blood vessels become thick and rigid (Wheater et al. 1985, p. 58). In arteriosclerosis, pathological changes in the blood vessel walls, such as stiffening or solidification, are caused, in part, by the unbalancing of components that make up the vessel wall (Stevens et al. 2002, p. 86). The most prevalent form of arteriosclerosis is known as atherosclerosis (Wheater et al. 1985, p. 58) that occurs in the walls of medium and large arteries (Stevens et al. 2002, p. 86), also known as the elastic and muscular arteries, respectively (Young et al. 2014, p. 148). Although atherosclerosis can occur in any of the arterial blood vessels, the arteries that tend to be targeted first include the renal, cerebral, iliofemoral (Stevens et al. 2002, p. 88), coronary, and carotid arteries, and the aorta (Damjanov et al. 2011, p. 2).

There are a variety of factors that influence the development of atherosclerosis (Damjanov et al. 2011, p. 2). As explained by Stevens et al. (2002, p. 86), the broad category of factors that make one more susceptible to atherosclerosis are known as constitutional factors, which are divided into two categories described as the major risk factors and the minor risk factors. Constitutional risk factors include increasing age, sex (males have a higher tendency to develop atherosclerosis than females), and genetic predispositions. Major risk factors include high levels of blood lipids, high blood pressure, smoking, and diabetes. Minor risk factors include a inadequate routine exercise, obesity, and high amounts of stress. Though atherosclerosis occurs to some degree in all human adults, and is the most prevalent form of arteriosclerosis, it is severe atherosclerosis that is of most concern (Stevens et al. 2002, p. 86).

Morphological changes in atherosclerotic tissue

Atherosclerosis development proceeds through a series of stages (Damjanov et al. 2011, p. 2): a fatty streak stage, a fibro-lipid plaque stage, and finally the complicated atheroma (Stevens et al. 2002, p. 87).

The beginning stage of atherosclerosis is known as the fatty streak stage (Figure 6) (Stevens et al. 2002, p. 87). It is characterized by the accumulation of lipids from the blood in the tunica intima (Damjanov et al. 2011, p. 2). These lipid components infiltrate the tunica intima through an injured endothelium. These lipids are primarily cholesterol, cholesterol esters, and triglycerides (Stevens et al. 2002, p. 87). This stage is also identified by the presence of a type of macrophage in the layers proximal to the lumen (Damjanov et al. 2011, p. 2). These macrophages appear foamy due to the amount of lipids they have phagocytosed (Damjanov et al. 2011, p. 2) and are therefore termed “foam cells” (Figure 7). These foam cells, which are thought to be the blood version of macrophages and myointimal cells, phagocytose most of the lipids, but still some lipids remain loose in the layer (Stevens et al. 2002, p. 87). These lipid molecules begin to aggregate in the tunica intima, after myointimal cells, so filled with lipids that they become malformed and distended, have apoptosed (Figure 8) (Stevens et al. 2002, p. 87).

The appearance of fatty streaks causes smooth muscle cells and fibroblasts to proliferate and attract more macrophages (Damjanov et al. 2011, p. 2). This next stage is referred to as the fibro-lipid plaque stage (Stevens et al. 2002, p. 87). In this stage, fibroblasts secrete growth factors, which contribute to the increase in collagen deposits (Figure 9) (Damjanov et al. 2011, p. 2). According to Stevens et al. (2002, p. 87), fibrocollagenous tissue is also made as a result of the accumulated lipid in the tunica intima. Macrophages release cytokines, which prompt myointimal cells to multiply. Some of these myointimal cells begin to synthesize collagen, which ultimately forms an enlarged collagen cap in the tunica intima. As this deposit continues to grow, the tunica media starts losing muscle cells, causing it to deteriorate (Figure 10) (Stevens et al. 2002, p. 87).

Once this part of the vessel wall progresses to the complicated atheroma stage, the intimal plaque is quite large (Stevens et al. 2002, p. 87). An atheroma is a result of the death of cells containing lipids, and the subsequent release of the lipids into the interstitial space. This atheroma lesion is a characterizing trait of atherosclerosis (Damjanov et al. 2011, p. 2). The tunica media has atrophied significantly, and collagen fibers have begun to replace the smooth muscle cells. The lipid aggregations in the intima tend to collect calcium salts, which accumulate and cause the plaque of fibrous collagen and lipid molecules to harden. Ulcers of the endothelium increase the likelihood of a thrombus attaching (Figure 11) (Stevens et al. 2002, p. 87).

Changes in Tissue Function manifested as symptoms

The thickening of the tunica intima associated with atherosclerosis can intrude into the lumen of the artery and hinder blood flow (Young et al. 2014, p. 148). Calcification and the formation of ulcers can continue to worsen atheromas (Damjanov et al. 2011, p. 2). Significant conditions that can result from atherosclerosis include occlusions, thrombosis, and and aneurysms (Stevens et al. 2002, p. 88). Occlusions refer to the reductions of the lumens of the blood vessels, caused by the thickening of the vessel walls (Stevens et al. 2002, p. 88). This can hinder or entirely prevent blood flow and circulation, and this reduced or blocked blood flow can result in the inadequate or complete lack of blood to the tissues the vessel provides for (Stevens et al. 2002, p. 88). The plaques can also burst, which would also contribute to blocking the luminal blood flow (Young et al. 2014, p. 148). According to Young et al. (2014, p. 148), the tunica intima can lose its characteristic smoothness and evenness. This change may allow platelets and fibrin to attach and form a thrombus, which would have otherwise be unable to stick to a smooth wall (Figure 11). This can also contribute to the plaque’s size and encroach on the lumen’s space (Young et al. 2014, p. 148). Ulcers in the endothelium may also lead to thrombosis (Stevens et al. 2002, p. 88). Pieces of the thrombus may break off and flow to smaller vessels and block them; these pieces are called emboli (Stevens et al. 2002, p. 88). The presence of atheroma in elastic arteries can result in the smooth muscle being replaced by collagen (Young et al. 2014, p. 148) and the loss of elastic fibers from the tunica media (Stevens et al. 2002, p. 88). This can weaken the blood vessel wall which can result in the billowing of the wall in that area – a phenomenon known as an aneurysm (Stevens et al. 2002, p. 88). If this bursts, this can result in a hemorrhage. Aneurysms may also precede thrombosis (Stevens et al. 2002, p. 88).

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