Atherosclerosis, Aneurysm, and Dissection PDF
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Batterjee Medical College
Yahya Al-Ghamdi
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This document provides an outline of atherosclerosis, aneurysm, and dissection. It covers definitions, risk factors, pathogenesis, and morphological changes, explaining the inflammatory process and impact on vascular health. The document also includes questions to test readers' understanding, and references for additional information.
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Atherosclerosis, Aneurysm and dissection Yahya Al-Ghamdi, MD Courtesy of Saeed Asiry, MD Outlines Definitions and risk factors Pathogenesis Morphological changes Clinical correlation Arteriolosclerosis Arteriosclerosis: hardening of the arteries generic term reflecting arter...
Atherosclerosis, Aneurysm and dissection Yahya Al-Ghamdi, MD Courtesy of Saeed Asiry, MD Outlines Definitions and risk factors Pathogenesis Morphological changes Clinical correlation Arteriolosclerosis Arteriosclerosis: hardening of the arteries generic term reflecting arterial wall thickening and loss of elasticity. Distinct clinicopathologic conditions: Atherosclerosis Arteriolosclerosis: affecting small arteries Mönckeberg medial sclerosis Atherosclerosis Characterized by intimal lesions called atheromas (or atheromatous or atherosclerotic plaques) that impinge on the vascular lumen and can rupture to cause sudden occlusion. Involves medium sized to large arteries It underlies the pathogenesis of coronary, cerebral, and peripheral vascular disease Atherosclerosis Characterized by intimal lesions called atheromas (or atheromatous or atherosclerotic plaques) that impinge on the vascular lumen and can rupture to cause sudden occlusion. Involves medium sized to large arteries It underlies the pathogenesis of coronary, cerebral, and peripheral vascular disease Atherosclerotic plaques Atheromatous plaque: Raised lesion with a soft core of lipid (mainly cholesterol and cholesterol esters) covered by a fibrous cap, often undergoes dystrophic calcifications Atherosclerotic plaques As atherosclerotic plague enlarge, they mechanically obstruct blood flow >>> stenosis Rupture of atherosclerotic plaque lead to obstructive thrombosis (the formation or presence of a blood clot in a blood vessel) https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.118.311098 Atherosclerotic plaques Atherosclerotic plaque can also increase the diffusion distance from the lumen to the media, leading to ischemic injury and weakening of the vessel wall, changes that may result in aneurysm formation (a ballooning at a weak spot in an artery wall. An aneurysm's walls can be thin enough to rupture) https://www.mayoclinic.org/diseases-conditions/brain-aneurysm/symptoms-causes/syc-20361483 Atherosclerosis – Risk Factors Pathogenesis Pathogenesis Endothelial cells injury and dysfunction, causing increased vascular permeability, leukocyte and platelets adhesion >>> inflammation Injured endothelial cells allow accumulation of lipoproteins Monocytes migration into the intima and transformation into macrophages and foam cells (lipid-laden macrophages) >>> inflammatory cytokines >> T-cells gets activated Smooth muscle cell produce extracellular matrix (collagen) Pathogenesis PDGF (from activated platelets, macrophages, endothelial cells, and smooth muscle cells): induce smooth muscle cell recruitment and proliferation Smooth muscle cell produce extracellular matrix (collagen) Morphology – Fatty Streaks https://webpath.med.utah.edu/CVHTML/CV114.html Fatty streaks: composed of lipid-filled foamy macrophages. Beginning as multiple minute flat yellow spots, they eventually coalesce into elongated streaks 1 cm long or longer Morphology – Fatty Streaks Fatty streaks: composed of lipid-filled foamy macrophages. Beginning as multiple minute flat yellow spots, they eventually coalesce into elongated streaks 1 cm long or longer Morphology – Atherosclerotic Plaque A. Atherosclerotic plaque (atheroma) B. Complicated lesions: - Ulceration (open arrow) - Thrombus (closed arrow) Morphology – Atherosclerotic Plaque Atherosclerotic plaques have three components: (1) cells: smooth muscle cells, macrophages, and T cells; (2) extracellular matrix, including collagen; and (3) intracellular and extracellular lipid Section stained with Elastic stain Inflammation, Section stained with Trichrome “stains elastic black” showing Calcifications (arrow head) stain “stains collagen blue”: C= attenuated/weakened elastic Neovascularization (arrows) central lipid core; F= fibrous cap; membranes L= residual lumen Atherosclerosis Consequences Atherosclerosis Consequences Atherosclerotic Stenosis (narrowing of lumen): In small arteries, atherosclerotic plaques can gradually occlude vessel lumina, compromising blood flow and causing ischemic injury Critical stenosis typically occurs at when the occlusion produces a 70% decrease in luminal cross-sectional area Atherosclerosis Consequences Rupture, ulceration and erosions: exposing highly thrombogenic plaque constituents (collagen) Hemorrhage into atheroma: rapidly expanding volume Atheroembolism: Plaque rupture can discharge atherosclerotic debris into the bloodstream, producing microemboli (free-floating debris that can block a distant artery) Aneurysm formation: Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness and potential rupture Plaque Consequences - Rupture Plaque rupture without superimposed Thrombosis superimposed on an thrombus. atherosclerotic plaque with focal disruption of the fibrous cap Aneurysm and dissection Aneurysm Aneurysm is dilation of blood vessels or heart Can eb congenital or acquired True aneurysm: Involves all 3 layers of the artery (intima, media, adventitia) E.g. atherosclerosis False aneurysm (pseudianeurysm): When wall defect leads to the formation of extravascular hematoma that communicates with intravascular space Aneurysm Dissection When blood gains entry through to the arterial wall through a surface defect and then pushes apart the underlying layers. Risk Factors and Pathogenesis Abnormal connective tissue synthesis: Marfan syndrome Ehler Danalos syndrome Weakening vessel wall: Atherosclerosis Hypertension Trauma Vasculitis Infections Abdominal Aortic Aneurysm Question A 70-year-old male smoker presents with sudden-onset abdominal pain and hypotension. Abdominal CT scan reveals a ruptured abdominal aortic aneurysm. What is the most common histopathological finding associated with the development of abdominal aortic aneurysms? A. Atherosclerosis B. Vasculitis C. Thrombosis D. Arterial dissection Arrow: calcifications Question A 63-year-old male with with a known history of HTN and DM came to the ER with crushing chest pain for 30 mins. ECG shows ST segment elevation. He was diagnosed with MI due to severe atherosclerosis of the coronary arteries. The earliest step in the development of atherosclerosis is: A. Accumulation of lipoproteins B. Monocyte adhesion to the endothelium C. Endothelial cells injury and dysfunction D. Activation of platelets Question What is the term for the detachment and movement of a piece of atherosclerotic plaque to a distant site in the circulation, potentially causing blockages in smaller vessels? A. Stenosis B. Embolism C. Thrombosis D. Aneurysm Question Where in the arteries does atherosclerosis primarily occur? A. Tunica externa B. Tunica media C. Tunica intima D. Tunica adventitia Question What is the primary component of the core of atherosclerotic plaques? A. Red blood cells B. White blood cells C. Fibrin D. Cholesterol and lipids Summary Atherosclerosis is a multifactorial chronic inflammatory process Initiated by endothelial cell injury with other cells playing big parts (macrophages and smooth muscle cells) Atheroma can lead to stenosis, rupture (thrombosis) with acute occlusion, hemorrhage, aneurysm formation and embolism References Kumar, Vinay; Abbas, Abul K.; Aster, Jon C.. Robbins Basic Pathology (Robbins Pathology) Elsevier Health Sciences. Pathoma Thank You Questions? [email protected]