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Atherosclerosis 3
 

Atherosclerosis 3

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this includes morpho,clinical features,complications,diagnosis,treatment....

this includes morpho,clinical features,complications,diagnosis,treatment....

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    Atherosclerosis 3 Atherosclerosis 3 Presentation Transcript

    • ATHEROSCLEROSIS MORPHOLOGY & COMPLICATIONS
      • S.SHRINATH
      • 83 Batch.
    •  
    • MORPHOLOGY
      • FATTY STREAK
      • ATHEROSCLEROTIC PLAQUE
    • -:FATTY STREAK:-
      • It is the earliest lesions in Atherosclerosis which is composed of foam cells.
      • Earlier formed as small flat yellow spots and then to a plaque.
      • Does not cause any obstruction to the blood flow.
    •  
    •  
    • -:ATHEROSCLEROTIC PLAQUE:-
      • Intimal thickening and lipid accumulation.
      • Lodged in the lumen of the artery (0.3-1.5 cm in dia).
      • Grossly they appear as white to yellow patches.
      • Lesions are mostly eccentric but rarely circumferential.
      • Local flow disturbances –increased susceptibility to plaque formation.
      • Most extensively affected vessels are:
        • Abdominal aorta
        • Coronary arteries
        • Popliteal arteries
        • Internal carotid arteries
        • Circle of willis
      • Components of Plaque:
      • Cells
              • T-cells
              • Smooth muscle cells
              • Macrophages.
      • ECM
              • Collagen
              • Elastic fibers
              • Proteoglycans
      • Lipids
              • Intracellular and extracellular.
      • -:DESCRIPTION – PLAQUE:-
      • Typically composed of superficial composed fibrous cap (smooth muscle cells and collagen).
      • Beneath it contains cellular area.
      • Deeply containing lipid core, cell debris, foam cells, fibrin, thrombus, plasma proteins.
      • Periphery shows neovascularisation.
    •  
      • -:NATURE OF THE PLAQUE:-
      • Progressively enlarges due to:-
          • Cell death and degeneration.
          • Synthesis and remodeling of collagen.
          • Organization of thrombus.
      • Often undergo calcification.
    •  
    •  
    •  
    • CHANGES IN THE ATHEROSCLEROTIC PLAQUE
      • Rupture ,erosion ,ulceration.
      • Hemorrhage into a plaque.
      • Atheroembolism.
      • Aneurysm formation.
    • RUPTURE
    • HEMORRHAGE INTO PLAQUE
    • ATHERO EMBOLISM
    • ANEURYSMS FORMATION
    • COMPLICATIONS
    • -:COMPLICATIONS:-
        • Myocardial infarction
        • Cerebral infarction (stroke).
        • Aneurysm
        • Peripheral vascular disease (PVD).
    • Atherosclerotic stenosis
      • Small arteries  plaques occlude lumen  compromising blood flow  ischemia.
      • Critical stenosis
          • Chronic occlusion significantly limits flow .
      • occurs at approx 70% occlusion in coronary circulation .
      • Consequences of stenosis
          • Mesenteric occlusion
          • and bowel ischemia.
          • Chronic IHD.
          • Ischemic encephalopathy.
          • Intermittent claudication.
    • ACUTE PLAQUE CHANGE
      • Partial or complete vascular thrombosis due to erosion or rupture of plaque resulting in acute tissue infarction.
      • Rupture  expose high thrombogenic substances.
      • Erosion  expose thrombogenic sub endothelial basement membrane.
      • Hemorrhage  expands the volume.
      • PLAQUE CONFIGURATION
      • Composition of plaque is dynamic .
      • Based on the plaque configuration it may be of stable or vulnerable.
      • Stable plaque
          • Thick fibrous cap
          • Small lipid core
      • Vulnerable plaque
          • Thin fibrous cap
          • Dense lipid core
    • EVENTS TRIGGERING CHANGES IN PLAQUE CONFIGURATION
      • INTRINSIC FACTORS - plaque structure and composition
      • Fibrous cap
            • Collagen (produced by smooth cells).
            • Collagen turnover is regulated by
            • Matrix metalloproteinase (macrophages within plaque),
            • Tissue inhibitors of metalloproteinase (endothelial cells,smooth muscle cells)
      • EXTRINSIC FACTORS -BP and platelet activity.
        • adrenergic stimulation  increase BP  increasing physical stress.
    • ROLE OF FREE RADICALS (OXIDATIVE STRESS) LDL Oxidised LDL Release of free radicals DAMAGE TO THE ARTERIAL WALL Into macrophages
    •  
      • THROMBOSIS
        • Partial or complete thrombosis associated with disrupted plaque is critical to the pathogenesis of acute stenosis.
        • Thrombosis is a potent activator of multiple growth related signals which contribute to the growth of atherosclerotic lesion.
      • VASOCONSTRICTION
      • This compromises lumen size and by increasing the local mechanical forces and can potentiate the plaque disruption .
    • CLINICAL FEATURES ON CORONARY ARTERIES:
      • Angina
      • Hyperhidrosis
      • Shortness of breath
      • Palpitations
      • Tachycardia
      • Weakness or dizziness
      • Nausea
      ON CAROTID ARTERIES:
      • Transient ischemic attacks
      • Dizziness ,Confusion ,Fainting , Coma
      • Loss of eyesight
      • Hemiplegia.
      • Claudication is the most common symptom of this condition . 
      • Pain
      • Coolness, numbness
      • Poor healing of wounds  
      • Ulcers leading to Gangrene formation
      • Black discoloration
      ON PERIPHERAL ARTERIES:
    • DIAGNOSIS
    • DIAGNOSIS SEROLOGICAL IMAGING LIPID PROFILE   HbA1c CRP-HS HOMOCYSTEINE LDL LEVEL LIPOPROTEIN a CT SCAN INTRAVASCULAR ULTRASOUND ANGIOGRAPHY DOPPLER STUDY
    • TREATMENT
    • TREATMENT NON-PHARMACEUTICAL PHARMACEUTICAL NON-FAT DIET CESSATION OF SMOKING REGULAR EXERCISE REDUCE ALCOHOL CONSUMPTION Use of drug surgical
    • PHARMACOTHERAPY DRUGS FOR REDUCING HYPERCHOLESTROLEMIA STATINS ATORVASTATIN FLUVASTATIN LOVASTATIN PRAVASTATIN SIMVASTATIN ROSUVASTATIN
      • USES OF STATINS
        • REDUCING PLAQUE SIZE.
        • STABILIZING PLAQUES.
        • DECREASING BLOOD CLOT FORMATION.
        • DECREASING CRP LEVELS.
    • DRUGS FOR REDUCING CLOT FORMATION VITAMIN –K ANTAGONIST WARFARIN ACENOCOUMAROL PHENINDIONE HEPARIN DERIVATIVES HEPARIN FONDAPARINUX INDRAPARINUX DIRECT THROMBIN INHIBITORS ARGATROBAN LEPIRUDIN BIVALURIDIN
      • THE DRUGS THAT BREAKSDOWN THE BLOOD CLOT
      • tissue plasminogen activator t-PA:
            • alteplase  ( Activase )
            • reteplase  ( Retavase )
            • tenecteplase ( TNKase )
      • antistreplase  ( Eminase )
      • streptokinase  ( Kabikinase ,  Streptase )
      • urokinase  ( Abbokinase )
    • SURGICAL INTERVENTION
      • BALOON ANGIOPLASTY AND STENTING
      • ATHERECTOMY
      • SURGICAL BYPASS
      • ENDATERECTOMY
    • SUMMARY
    • MORPHOLOGY
    • MORPHOLOGY
    • COMPLICATIONS MYOCARDIAL INFARCTION STROKE PERIPHERAL VASCULAR DISEASE ANEURYSM FORMATION
    • COMPLICATIONS Atherosclerotic stenosis
      • Critical stenosis
      • Consequences of stenosis
      Acute plaque change
      • Stable plaque & vulnerable plaque
      • Factors that bring about the Change.
    •  
    • THANK YOU