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Sruthi

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    Sruthi Sruthi Presentation Transcript

    • BY SRUTI MARY JOSEPH
    • ATHEROSCLEROSIS
      • Atherosclerosis is a specific form of arteriosclerosis (thickening & hardening of arterial walls) affecting primarily the intima of large and medium-sized muscular arteries and is characterized by the presence of fibro fatty plaques or atheromas.
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    • ATHEROSCLEROSIS
      • Most commonly affected arteries by atherosclerosis include large and medium sized arteries like aorta , coronary , popliteal and cerebral arteries .
      • Major complications resulting from ischemia due to atherosclerosis include myocardial infarction leading to heart attacks and cerebral infarction leading to strokes .
      • Less common complications include peripheral vascular disease, aneurysmal dilatation due to weakened arterial wall, chronic ischemic heart disease, ischemic encephalopathy and mesenteric occlusion.
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    • PATHOGENESIS OF ATHEROSCLEROSIS
      • INSUDATION HYPOTHESIS
      • Put forth by Virchow in 1852 stating that Atherosclerosis is a form of cellular proliferation of the intimal cells resulting from increased imbibing of lipids from the blood. Earlier known as “lipid theory” is now called “response to injury hypothesis” and is the most widely accepted theory.
      • ENCRUSTATION HYPOTHESIS
      • Put forth by Rokitansky in 1852 stating that atheroma represented a form of encrustation on the arterial wall from the components in the blood forming thrombi composed of platelets, fibrin and leucocytes, and was earlier named as “thrombogenic theory”.
    • RESPONSE TO INJURY THEORY
      • Original theory put forth in 1973 modified in 1993.
      • Original Theory: Initial event in atherogenesis is endothelial injury followed by smooth muscle cell proliferation. As per this theory early lesions mainly consist of smooth cells.
      • Modified theory describes lipoprotein entry into the intima as the initial event followed by lipid accumulation in the macrophages (now foam cells) which according to modified theory are the dominant cells in early lesions.
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    • EVENTS
      • Endothelial injury
      • Accumulation of lipoprotein (mainly LDL)
      • Monocyte adhesion to the endothelium
      • Transformation of monocytes into macrophages & foam cells
      • Platelet adhesion
      • Smooth muscle cell recruitment, proliferation &ECM production
      • Lipid accumulation both extracellularly &within cells
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    • ENDOTHELIAL INJURY
      • Endothelial Injury :
        • Initial triggering event in the development of Atherosclerotic lesion
        • Caused due to chronic hyperlipidaemia, homocystine, circulating toxins from systemic infections, viruses, hypoxia, radiation, carbon monoxide and tobacco products.
        • In man, two major risk factors are haemodynamic stress from hypertension and chronic hyperlipidaemia.
    • ROLE OF LIPIDS
      • The mechanism by which hyperlipidemia contributes to atherogenesis include:
      • Impairment of EC function through increased production of oxygen free radicals that deactivate NO: the major Endothelial Relaxing Factor
      • Oxidised lipid generated by free radicals is ingested by by monocytes via the scavenger receptor distinct from the LDL receptor thus forming FOAM cells
    • CONT’D
      • Increases monocyte accumulation in lesion
      • Stimulates release of Growth Factors & Cytokines
      • Cytotoxic to EC & SMC
    • ROLE OF SMOOTH MUSCLE
      • Intimal Smooth Muscle Cell Proliferation
        • Endothelial injury causes adherence and aggregation of platelet at the site.
        • Proliferation of intimal smooth muscle cells is stimulated by various mitogens released from platelets adherent at the site of endothelial injury.
        • These mitogens include PDGF, fibroblast growth factor, TGF- ά .
        • Proliferation is also facilitated by nitric oxide and endothelin released from endothelial cells.
    • ROLE OF BLOOD MONOCYTES
    • ROLE OF HYPERLIPIDEMIA
      • 4. Role of Hyperlipidaemia
        • Chronic hyperlipdaemia in itself may initiate endothelial injury.
        • Increased serum concentration of LDL and VLDL promotes formation of foam cells.
        • while high serum concentration of HDL has anti-atherogenic effect.
    • ROLE OF INFLAMATION
      • Upregulation of endothelial adhesion molecules VCAM which binds monocytes & T cells
      • After adhering to the endothelial cell, monocytes between the cells stimulated by chemokines & transform into macrophage, that engulf oxidised LDL
      • Macrophages contribute to the growth of lesion by:
      • Producing IL-1 & TNF which increases adhesion of leukocytes
    • CONT’D
      • Produce chemokines eg:MCP-1
      • Produce reactive oxygen species which causes oxidation of LDL in the lesion.
    • ROLE OF THROMBOSIS
        • Endothelial injury exposes sub-endothelial connective tissue resulting in platelet aggregation at the site besides proliferation of smooth muscle cells.
        • This causes mild inflammatory reaction which together with foam cells is incorporated into atheromatous plaque.
        • Lesions enlarge by attaching fibrin and blood cells causing thrombus formation which becomes a part of atheromatous plaque.
    • ROLE OF INFECTION
      • Infection mainly due to CHLAMYDIA PNEUMONIA also lead to atherosclerosis.
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