Cardiac Disease Table.docx - Cardiovascular Disorders and Murmurs Disease Condition ATHEROSCLEROSIS Etiology Pathophysiology Pathogenesis Clinical

Cardiac Disease Table.docx - Cardiovascular Disorders and...

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Cardiovascular Disorders and Murmurs Disease/ Condition Etiology/ Pathophysiology/ Pathogenesis Clinical Manifestations Labs/Other Studies Other pertinent info ATHEROSCLEROSIS Arteriosclerosis is an inflammatory disease that causes hardening of the arteries. o Atherosclerosis is soft deposits of intra-arterial fat and fibrin that collect and harden over time. The most common form of arteriosclerosis is atherosclerosis. 50% for the risk for atherosclerosis is attributed to genetics – many of these genes are associated with inflammation seen in atherosclerosis Pathopysiology of atherosclerosis The plaques of atherosclerosis develop in medium and large sized arteries. The process is initiated by endothelial surface damage/injury to the arterial intima layer (interior lining of the artery) → initiating an inflammatory response and increasing vessel wall permeability → The injury allows low density serum lipoproteins to breach the tunica intimal layer of the arteries → Leukocytes and endothelial cells oxidize these lipids and produce further damage → Platelets aggregate at the site and release platelet derived growth factors which stimulate growth of smooth muscle cells → Medium smooth muscle cells normally confined to outer layers of the artery are drawn to the intima where they proliferate --> The result is atherosclerotic plaque, primarily composed of smooth muscle cells, lipoproteins, and inflammatory debris → Plaque slowly enlarge and the interior diameter of the artery is decreased and perfusion to the tissues is diminished → decreased blood flow and ischemia to that tissue. o This can lead to cardiac, renal, peripheral artery disease, stroke, MI, and other complications. It may also cause HTN because of the narrowing of arteries. o Conversely, HTN is also one factor that may cause injury that initiates atherosclerosis. Foam Cells 1. When there are a large number of LDL/VLDL particles (hypercholesterolemia) present, they can breach the endothelial lining of the artery into the intima of the artery → inflammatory response which call monocytes → monocytes adhere to the lining and then move inside artery (thus becoming macrophages) → macrophages engulfs the oxidized LDL and becomes a foam cell that reside just under the endothelium→ Foam cells release cytokines → change the smooth muscle and encourages atherosclerosis as well as creates a growing lipid pool at the intima. Progression of atherosclerosis All of these changes begin with a damaged endothelium. Chronic endothelial injury may be caused by HTN, smoking, hyperlipidemia, hyperhomocysteinemia, hemodynamic factors, toxins, viruses, and immune factors. The normal artery is smooth. The endothelium lining is the innermost, followed by the tunica intima, then the tunica media which is all surrounded by the adventitia (the outermost layer) Once there is an injury to the endothelial lining there is an inflammatory response → platelets start to aggregate → emit
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