Clinical I: Coronary and Peripheral Circulation PDF
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This document provides an overview of coronary and peripheral circulation. It covers atherosclerosis, including its formation and biology, and relates it to coronary circulation and peripheral vascular diseases, such as angina pectoris. The text also details cell biology behind atherosclerosis.
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17/03/24 Clinical I: Coronary and Peripheral circulation Learning objective: explain what a atherosclerosis is and occlusion including its formation. Learning objective: explain the cell biology of a atherosclerosis and its formation and common locations. Learning objective: de ne how the above rela...
17/03/24 Clinical I: Coronary and Peripheral circulation Learning objective: explain what a atherosclerosis is and occlusion including its formation. Learning objective: explain the cell biology of a atherosclerosis and its formation and common locations. Learning objective: de ne how the above relates to coronary circulation. Learning objective: illustrate the different parts of coronary angiograms. Learning objective: de ne what is meant by peripheral vascular disease. Atherosclerosis: Is a disease characterised by the formation of plaques in the intima of large and medium-sized arteries. Plaques alone are usually benign, even when present in large numbers throughout the arterial system. However, life-threatening ischaemic damage to vital Blocking organs may occur when an occlusive thrombus forms on a spontaneously disruptive plaque. These acute obstructions can occur in many different arteries, resulting in a wide range of clinical disorders. Cell biology behind this: The formation of lesions starts in young children, especially in society with a high dietary fat intake. The earliest signi cant lesion is called a fatty streak. Fatty streaks consist of lipid-containing foam cells in the arterial just beneath the endothelium. Overtime, they can evolve into atherosclerotic plaques or remain stable or even regress. Biology of atherosclerosis (1): Injury to the endothelium triggers monocyte adhesion, a loosening of endothelial cell junctions and migration of monocytes beneath the endothelium, where they differentiate into macrophages. The more permeable endothelium also permit LDL to enter the intima of the artery and macrophages begin engul ng the LDL by phagocytosis. After macrophages become laden with lipid from ingesting LDL, they are referred to as foam cells. Biology of atherosclerosis (2): The diagram also shows the role of T lymphocytes, which are also in the intima. They secrete cytokines that eventually induced smooth muscle cells to migrate from the media into the intima. The smooth muscle cells also begin to proliferate under the in uence of growth factors. Overtime, there is a progressive accumulation of lipid and smooth muscle cells in the intima. Eventually, the growing lesion begins to raise the endothelium and encroach on the lumen of the artery. The lesion is now known as an atherosclerotic plaque. Stable and unstable plaques: Atherosclerotic plaques evolve in 2 possible ways. 1. Slowly growing plaques expand gradually due to the accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells. These plaques tend to stabilise and are not prone to rupture. A brin cap forms. 2. In contrast, other the plaques grow more rapidly as a result of more rapid lipid deposition. These have thin brin caps that are prone to rupture. Once a plaque ruptures, it can trigger an acute thrombosis by activating platelets and the clotting cascade. Coronary heart disease: Stable Angina Pectoris: In coronary arteries, atherosclerotic narrowing that reduces the lumen of a coronary artery by more than 75% causes angina pectoris, the chest pain that results when pain-producing substances accumulate in the myocardium. Typically, the pain comes on during exertion and disappears with rest, as a substances are washed out by the blood. Unstable Angina Pectoris: If a plaque is unstable and becomes disrupted, then 2 things can happen: 1. A mural thrombus forms on top of a ruptured plaque. A mural thrombus is one where the thrombus is in contact with the endocardial lining of a large blood vessel, such as an artery, but is not occlusive. This causes variable obstruction of the coronary artery leading to pain at rest or minimal exertion. 2. A thrombus forms on top of a ruptured plaque and occludes the lumen of the coronary artery, leading to death of full thickness of cardiac muscle supplied by that artery. Peripheral vascular disease or Peripheral arterial disease: PAD is the presentation that results when atherosclerosis of the arteries of the lower legs cause symptoms of ischaemia and/or infarction to occur. If the circulation of a limb is severely compromised, the skin can ulcerate, producing lesions that are slow to heal.