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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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  • 1. ATHEROSCLEROSIS MORPHOLOGY & COMPLICATIONS
    • S.SHRINATH
    • 83 Batch.
  • 2.  
  • 3. MORPHOLOGY
    • FATTY STREAK
    • ATHEROSCLEROTIC PLAQUE
  • 4. -: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.
  • 5.  
  • 6.  
  • 7. -: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.
  • 8.
    • Most extensively affected vessels are:
      • Abdominal aorta
      • Coronary arteries
      • Popliteal arteries
      • Internal carotid arteries
      • Circle of willis
  • 9.
    • Components of Plaque:
    • Cells
            • T-cells
            • Smooth muscle cells
            • Macrophages.
    • ECM
            • Collagen
            • Elastic fibers
            • Proteoglycans
    • Lipids
            • Intracellular and extracellular.
  • 10.
    • -: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.
  • 11.  
  • 12.
    • -:NATURE OF THE PLAQUE:-
    • Progressively enlarges due to:-
        • Cell death and degeneration.
        • Synthesis and remodeling of collagen.
        • Organization of thrombus.
    • Often undergo calcification.
  • 13.  
  • 14.  
  • 15.  
  • 16. CHANGES IN THE ATHEROSCLEROTIC PLAQUE
    • Rupture ,erosion ,ulceration.
    • Hemorrhage into a plaque.
    • Atheroembolism.
    • Aneurysm formation.
  • 17. RUPTURE
  • 18. HEMORRHAGE INTO PLAQUE
  • 19. ATHERO EMBOLISM
  • 20. ANEURYSMS FORMATION
  • 21. COMPLICATIONS
  • 22. -:COMPLICATIONS:-
      • Myocardial infarction
      • Cerebral infarction (stroke).
      • Aneurysm
      • Peripheral vascular disease (PVD).
  • 23. 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.
  • 24. 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.
  • 25.
    • 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
  • 26. 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.
  • 27. ROLE OF FREE RADICALS (OXIDATIVE STRESS) LDL Oxidised LDL Release of free radicals DAMAGE TO THE ARTERIAL WALL Into macrophages
  • 28.  
  • 29.
    • 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.
  • 30.
    • VASOCONSTRICTION
    • This compromises lumen size and by increasing the local mechanical forces and can potentiate the plaque disruption .
  • 31. 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.
  • 32.
    • 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:
  • 33. DIAGNOSIS
  • 34. DIAGNOSIS SEROLOGICAL IMAGING LIPID PROFILE   HbA1c CRP-HS HOMOCYSTEINE LDL LEVEL LIPOPROTEIN a CT SCAN INTRAVASCULAR ULTRASOUND ANGIOGRAPHY DOPPLER STUDY
  • 35. TREATMENT
  • 36. TREATMENT NON-PHARMACEUTICAL PHARMACEUTICAL NON-FAT DIET CESSATION OF SMOKING REGULAR EXERCISE REDUCE ALCOHOL CONSUMPTION Use of drug surgical
  • 37. PHARMACOTHERAPY DRUGS FOR REDUCING HYPERCHOLESTROLEMIA STATINS ATORVASTATIN FLUVASTATIN LOVASTATIN PRAVASTATIN SIMVASTATIN ROSUVASTATIN
  • 38.
    • USES OF STATINS
      • REDUCING PLAQUE SIZE.
      • STABILIZING PLAQUES.
      • DECREASING BLOOD CLOT FORMATION.
      • DECREASING CRP LEVELS.
  • 39. DRUGS FOR REDUCING CLOT FORMATION VITAMIN –K ANTAGONIST WARFARIN ACENOCOUMAROL PHENINDIONE HEPARIN DERIVATIVES HEPARIN FONDAPARINUX INDRAPARINUX DIRECT THROMBIN INHIBITORS ARGATROBAN LEPIRUDIN BIVALURIDIN
  • 40.
    • 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 )
  • 41. SURGICAL INTERVENTION
    • BALOON ANGIOPLASTY AND STENTING
    • ATHERECTOMY
    • SURGICAL BYPASS
    • ENDATERECTOMY
  • 42. SUMMARY
  • 43. MORPHOLOGY
  • 44. MORPHOLOGY
  • 45. COMPLICATIONS MYOCARDIAL INFARCTION STROKE PERIPHERAL VASCULAR DISEASE ANEURYSM FORMATION
  • 46. COMPLICATIONS Atherosclerotic stenosis
    • Critical stenosis
    • Consequences of stenosis
    Acute plaque change
    • Stable plaque & vulnerable plaque
    • Factors that bring about the Change.
  • 47.  
  • 48. THANK YOU

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