Similarity between the Pathological Processes in the Body and the CNS - Essay Example

Similarity between the pathological processes in the body and the CNS al affiliation The human body is organised into various systems which work in interdependently but with similar pathological processes. In respect to multiple sclerosis and atherosclerosis, the nervous system which is divided into the central nervous system and the peripheral nervous system and the cardiovascular system are explored to determine if the pathological processes are similar (Khurana, 2008). The Central Nervous System (CNS) is protected by the cranium and the vertebral column and consists of the brain and the spinal cord. The brain integrates sensory information and coordinates body functions while the spinal cord enables transmission of signals between the brain and the rest of the body. The CNS is connected to the other parts by bundles of axons called axons. Axons are located in the white matter while the cell bodies of neurons in the CNS are in regions referred to as the gray matter (Kiernan & Rajakumar, 2013). Other than the neurons, the central nervous system has four types of glial cells, the oligodendrocytes, microglia, astrocytes and ependymal cells. Oligodendrocytes ensure myelination in the CNS and hold axons together. The microglia are macrophages and their function is to remove foreign matter such as pathogens. The ependymal cells are epithelial cells lining the internal surface of the ventricle and the CNS therefore acting as barrier between the nervous system and the fluid in the cavities. The astrocytes provide support by holding cell bodies and axons and also regulate nutrition and metabolic processes (Palastanga & Soames, 2012). Multiple sclerosis is a chronic relapsing demyelinating inflammatory disease of the central nervous system. The glial and neuronal components of the central nervous system are destructed by the inflammatory and the immunomediated processes. Formation of disseminated focal lesions in the gray and white matter of the brain and the spinal cord leading to destruction of oligodendrocytes, axon loss and degeneration, demyelination of axons and neuronal damage (Kesselring, et al., 2010). Below are two diagrams that show a norma myelin sheath and one under that is demyelinated. Figure 1: A normal myelin sheath Figure 2: Progression of demyelination of the myelin sheath The cardiovascular system has blood vessels which are are classified into arteries, resistance vessels, and capillaries. In a normal artery wall it is composed of two layer; the intima and the media. The intima is made up of a single layer of endothelial cells that are seated on basement membrane then the internal elastic lamina. Beneath the internal elastic lamina is the medial layer consisting the vascular smooth muscle cells surrounded by basement membrane and embedded in interstitial extracellular matrix. The boundary of the media marked by external elastic lamina. Atherosclerosis is a cardiovascular disease caused by ischemic complications of arterial atherosclerotic plaques manifested primarily through sudden cardiac death, acute coronary syndromes and stroke leading to death and disability due to limited blood flow in the tissues due to luminal reduction. Atherosclerosis is majorly localised to the intima and the immediate area surrounding the internal elastic lamina of primarily medium and large sized arteries. (Maciejko, 2004). Factors that are associated in progress of atherosclerosis include vascular inflammation, cholesterol, and arterial smooth muscle (MccConnell, 2007). Below are two diagrams that show a normal and healthy artery and an artery affected by artherosclerosis. Figure 3: Normal artery Figure 4: An atherosclerotic plaque In multiple sclerosis the formation of disseminated focal lesions in gray and white matter of the brain and the spinal cord characterised by destruction of oligodendrocytes, axon loss and degeneration, demyelination of axons and neuronal damage. (Kesselring, et al., 2010) Atherosclerosis is also characterised by formation of lesions. This is due to endothelial dysfunction which permits entry of lipids and inflammatory cells into the arterial wall. The lesions progress into larger plaques due to the formation of necrotic core and fibrous cap (John & Johnson, 2010). Therefore both diseases are characterised by formation of lesions. In multiple sclerosis, macrophages usually consume and digest the myelin basic protein released during the destruction of the myelin. The macrophages are recruited by bringing in monocytes in the blood. The degeneration of the myelin sheath and axonal damage slows down action potential down the axons (Lezzoni, 2010). During the destruction of myelin, two processes are involved. Phagocytic cells may interact with myelin sheaths and take up small fragments of myelin. This means that the sequence of demyelination, myelin is attacked by macrophages. In other instances, invasion of macrophages can be seen especially if the inflammatory process is extensive and severe. The myelin fragments which are taken up in macrophages are degraded within the cell to cholesterol esters and triglycerides (Kesselring, 1997). In atherosclerosis, monocytes in the artery differentiate into macrophages which take up lipid and form cell macrophages in the intima. The lesions progress into larger plaques due to the formation of necrotic core and fibrous cap. The cell macrophages engorged in lipid die and release their contents contributing to the formation of necrotic core. Inflammation is induced due to the accumulation of extracellular lipids and growth factors (John & Johnson, 2010). In conclusion, macrophages are involved in formation of the lesions in both diseases. In multiple sclerosis, the glial and neuronal components of the central nervous system are destructed by the inflammatory and the immunomediated processes leading to slow transmittance of signals in the neurons (Kesselring, et al., 2010). During the first stages of atherosclerosis, the growth of most plaques is abluminal or into the artery wall through positive remodelling. This enlarges the outer diameter of the vessel in attempt to by the artery to preserve the normal lumen size and blood flow. As the atherosclerotic process advances some plaques grow inwards into the lumen of the vessel leading to stenosis and this is referred to as negative remodelling (Maciejko, 2004). Demyelination and growth of plaques in the arteries, both impede transmission of substances that is transmission of signals in multiple sclerosis and blood flow in the local body organs in atherosclerosis. Both multiple sclerosis and atherosclerosis show similar disease progression. The lesions advance and form larger lesions which are referred to as plaques in atherosclerosis. In multiple sclerosis the lesions undergo distinct stages from an early stage when the myelin is actively destroyed to an inactive stage. A pre-active lesion is activated in a normal myelin and no abnormalities can be detected in the tissue but immune - histological studies would indicate stress on oligodendrocytes. The pre-active lesions advance to active lesions. In this stage, lymphocytes are present in the perivascular space. The active lesion progresses to a chronic active lesion in which at the centre of the lesion, myelin is completely absent due to clearance of macrophages. Foamy macrophages may be observed at the edge of the demyelinated centre. The chronic active lesion advances to the chronic inactive lesion which is grey, sunken, sclerotic lesion. The lesion is demyelinated, hypo cellular, densely gliotic. Astrocytes and oligodendrocytes are absent (Atkins, 2012). In atherosclerosis, the early asymptomatic lesions both the intimal thickening and intimal xanthomas are the earliest stage of the disease. The intimal mass lesion in the intima serves as precursor of advanced atherosclerotic lesions. The lesions referred to as fatty streaks are small, slightly raised lesions caused by focal collections of foam cell macrophages in the intima. The lesion progresses to form a necrotic core and a fibrous cap. The formation of the necrotic core is due to cell macrophages that die in the lipid therefore releasing contents. Formation of fibrous cap is due to vascular smooth muscle cell migration into the intima where they proliferate and deposit extracellular matrix. The increase in cell number and presence of matrix causes augmentation of bulk plaque which protrudes into the lumen (John & Johnson, 2010). The symptoms of multiple sclerosis are a result of white matter of the central nervous system. The initial symptoms begin with numbness in the limbs, visual loss, slowly developing motor onset, diploma, acutely evolving motor dysfunction, vertigo, bladder symptoms, and heat and exercise intolerance. (Burks & Johnson, 2000) In multiple sclerosis, the physical symptoms include elevated blood pressure and signs of hyperlidemia such as arcus senilis and xanthoma in some patients. Later, advancement in atherosclerotic changes cause an imbalance between oxygen supply and demand to the myocardium, shortness of breath, exercise intolerance, and exercise induced myocardial ischemia (Bricker, et al., 2004). In conclusion, the central nervous system and the body in reference to the cardiovascular system have similar to pathological processes. This can be inferred from similarity in the progression and manifestation of multiple sclerosis and atherosclerosis. Both diseases have similar development of lesions, progression of lesions to plaques and presence of macrophages in the advancement of the disease. References Atkins, G. J., 2012. The biology of multiple sclerosis. New York: Cambridge University Press. Bricker, S. L., Langlais, R. P. & Miller, C. S., 2004. Oral diagnosis, oral medicine,and treatment planning. 2nd ed. Hamilton: B.C Decker. Burks, J. S. & Johnson, K. P., 2000. Multiple sclerosis : diagnosis, medical management, and rehabilitation. New York: Demos. John, S. J. & Johnson, J., 2010. Atherosclerosis: molecular and cellular mechanisms. Weinheim: Wliey VCH. Kesselring, J., 1997. Multiple sclerosis. New York: Cambridge University Press. Kesselring, J., Comi, G. & Thompson, A. J., 2010. Multiple sclerosis : recovery of function and neurorehabilitation. New York: Cambridge,U.K. Khurana, I., 2008. Essentials of Medical Physiology. India: Elsevier. Kiernan, J. & Rajakumar, R., 2013. Barrs: The Human Nervous System: An Anatomical Viewpoint. 10th ed. Philadelphia: Lippincott Williams & Wilkins. Lezzoni, L. I., 2010. Multiple sclerosis. Santa Barbara, Calif: Greenwood. Maciejko, J. J., 2004. Atherosclerosis risk factors. Washington, DC: AACC Press. MccConnell, T. H., 2007. The nature of disease: pathology for the health professions. Baltimore: Lippincott Williams &Wilkins. Palastanga, N. & Soames, R., 2012. Anatomy and human movement: structure and function. 6th ed. Edinburgh: Churchill Livingstone. Read More