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