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13- Cardiovascular Pathology .docx

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McGill University
PATH 300
Edith Zorychta

Cardiovascular Pathology 1 Disorders of Blood Vessels Atherosclerosis is #1 cause of death in Canada. It impairs supply of blood to organ, leading to  Myocardial infarct  Stroke  Aneurysm (weakening of vessel wall)  Peripheral vascular disease (impaired blood flow to legs for example) Pathological change in the wall of the artery. 3 components  Intima- endothelial cells with some smooth muscle cells  Media- thicker, with smooth muscle  Adventitia- connective tissue, sympathetic nerve supply The cells involved are the endothelial and smooth muscle cells. This disease is slow and predictable. Starts early at 20 years old. 1. Early- fatty streak with some foam cells. 2. Onset- characterized by a variable fibrous plaque (not blocking) 3. Advanced lesion- narrowing of lumen and decrease in blood flow. Risk of complications including hemorrhage, ulceration, thrombosis blocking entire flow of blood. a. Infarct if blood flow blocked to heart, brain, or periphery. Clinical manifestations of atherothrombosis (major problem) Warning symptoms Immediate Transient ischemic attack Ischemic stroke Angina (chest pain due to ischemia of the Myocardial infarct heart, generally obstruction of coronary artery) Peripheral arterial disease (only feel pain if moving). Pathogenesis Largely preventable, multifactorial risk (harder to determine the different components of risk). Key components were found to be endothelial dysfunction and chronic inflammation. 1) Hemodynamic stress 2) Cell mediators/cytokines act on arterial wall 3) Lipoprotein entry and accumulation Molecular level  Initial event is damage to the endothelium o (1) Hemodynamic stress: Branches experience more blood pressure it and you're at a greater risk of atherosclerosis  Platelet aggregation (incredibly active in inflammation) o Platelets, leukocytes, mediators plaque begins to form. Macrophages go into wall of vessel and turn into foam cells. Lipid accumulates here too. Platelet aggregations release GF which leads to a proliferation of smooth muscle cells.  Migration of smooth muscle cells into the intima. o (2) Platelet aggregations release GF which affect smooth muscle. The macrophages in the wall releases GF. Fibroblasts live in the wall, and they release GF. Lymphocytes come in to site of injury and release GF. o Tons of cytokines trigger the growth and proliferation, migration of smooth muscle cells. Also smooth muscle change their properties and synthesize ECM.  Components come into an make plaque Macrophages receive signals from smooth muscle and T cells. Once macrophage is in the wall, it takes up lipids. Foam cells = macrophages filled with lipid (3) Lipoprotein consists of phospholipid/cholesterol/apoprotein on outside, triglyceride/cholesterol esters on inside.  Chylomicrons: formed from absorption of nutrients  LDL vs HDL: HDL has more protein and less cholesterol, while LDL is high in cholesterol and lipids o VLDL made in liver. In the circulation it delivers up lipids to periphery.  LDL delivers cholesterol. High levels of LDL = high levels of cholesterol forming atherosclerotic plaque. Enters wall where there's damage and oxidized. Scavenger receptors pick up oxidized LDL, like the macrophage which picks it up forming foam cells. Macrophage is releasing inflammatory cytokines.  HDL removes cholesterol from tissues (protective). Keeps cholesterol levels low in tissues and circulation. A diet full of lipid will promote the vessel to take up LDL and hypercholesterolemia occurs. Monocytes attach and migrate from media. Fatty streaks contain foam cells. Smooth muscles cells  Accumulate lipidbecome foam cells, and also synthesize collagen, elastin and glycoproteins.  Can change from contractile to synthetic state. Now it can release collagen and form a fibrous coating on the surface of the plaque. Other cells from other locations  Stem cells from bone marrow that become progenitor cells for smooth muscle or endothelium are involved.  Formation of a fibrous cap over the top of the plaque. Can be stabilizing because prevents rupturing. Stable vs unstable plaques depend on fibrous cap o Stable: thick cap, hard core o Unstable: thin cap, soft core  If plaque ruptures, materia
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