Atherosclerosis

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Background, Pathogenesis, Morphology, Treatment

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Atherosclerosis

  1. 1. “Arteries are blood vessels that carry oxygen andnutrients from your heart to the rest of your body.Healthy arteries are flexible and elastic. Over time,however, too much pressure in your arteries can makethe walls thick and stiff — sometimes restricting bloodflow to your organs and tissues.” This process is called arteriosclerosis, or hardening of the arteries.
  2. 2. Coverage:
  3. 3. o specific type of arteriosclerosis o a.k.a arteriosclerotic vascular disease or ASVD“athere” - deposition within the walls of arteries“sclerosis” - hardeningo luminal narrowing of arterieso caused by the formation of multiple plaques within the arteries lipid and fibrous material between the intimal and medial layers of the vessel
  4. 4. FACTORS that increase the risk of Coexisting conditions: Lifestyle, social and environmental factors: Permanent Hypertension 1. factors: 1. Cigarette Smoking 1.2.2. Diabetes mellitus Age of physical activity Lack 2. Family history of early heart disease 3. 3. Hyperlipidemia* Diet 4. Obesity*elevated concentrations of the lipids in the blood (LDL and HDL)
  5. 5. Other Factors That AffectSleep apnoea - a disorder in which the breathing stops or gets very shallow while aBlood is sleeping person pressureStress - emotionally upsetting event-particularly one involving anger.Alcohol - heavy drinking can damage the heart muscle and worsen other risk factors for atherosclerosis
  6. 6. Philippines Statistics  90% of Filipino adults have at least one risk factor to atherosclerosis.  identified risk factors were dyslipidemia, diabetes, hypertension, smoking and obesity. (NUTRITION AND HEALTH STATUS OF FILIPINO ADULTS)United States statistics ̴ 80 million people, or 36.3% of the population have CVD ̴ 14 million persons No. 1 cause of death for men and women in the US responsible for approximately 20% of all US deaths.
  7. 7. The elderly and Atheriosclerosis disease: Age is the strongest risk factor for the development of Atherosclerosis. clinically apparent in patients aged 40 years or older, but elderly persons experience higher mortality and morbidity rates from it. ̴ 82% of people who die of Atherosclerosis are 65 years or older. “Although atherosclerosis usually manifests in later life, its early phases are present in teenagers and young adults.” tc. healthy lifestyle!
  8. 8. © CBBitangcor Presentations
  9. 9. © CBBitangcor Presentations
  10. 10. © CBBitangcor Presentations
  11. 11. © CBBitangcor Presentations
  12. 12. Fatty Streaks• composed of lipid-filled foam cells but are not significantly raised• begin as multiple minute yellow, flat spots that can coalesce into elongated streaks, 1 cm long or longer
  13. 13. Fatty Streaks • can appear in the aortas of infants younger than 1 year and are present in virtually all children older than 10 years Aorta with fatty streaks (arrows), associated largely with the ostia of branch vessels
  14. 14. Fatty streak in an experimental hypercholesterolemicrabbit, demonstrating intimal, macrophage-derived foamcells (arrow).
  15. 15. Atherosclerotic Plaque• Atheromatous plaques (also called fibrous or fibrofatty plaques) impinge on the lumen of the artery and grossly appear white to yellow• thrombosis superimposed over the surface of ulcerated plaques is red- brown in color• 0.3 to 1.5 cm in diameter but can coalesce to form larger massesAtherosclerotic lesions• patchy, usually involving only a portion of any given arterial wall• appear "eccentric"
  16. 16. Atherosclerotic plaques three principalcomponents: (1) cells, including SMCs, macrophages, and T cells (2) ECM, including collagen, elastic fibers, andproteoglycans(3) intracellular and extracellular lipid
  17. 17. A. Fibrous cap is composed of SMCs and relatively dense collagen. Beneathand to the side of the cap(the "shoulder") is a more cellulararea containing macrophages,T cells, and SMCs.
  18. 18. B. Necrotic core, containing lipid (primarily cholesterol and cholesterol esters), debris from dead cells, foam cells (lipid- laden macrophages and SMCs), fibrin, variably organized thrombus, and other plasma proteins; the cholesterol content is frequently present as crystalline aggregates that are washed out during routine tissue processing and leave behind only empty "clefts.“- Deep to the fibrous cap
  19. 19. C. Neovascularization (proliferating smallblood vessels) at the periphery of thelesions Higher magnification photomicrograph at the junction of the fibrous cap and core, showing scattered inflammatory cells, calcification (arrowhead), and neovascularization (small arrows).
  20. 20. Atherosclerotic plaques are susceptible to the following pathologicchanges with clinical significance: Rupture, ulceration, or erosion of the luminal surface of atheromatousplaques exposes the bloodstream to highly thrombogenic substancesand induces thrombus formation. Such thrombi can partially orcompletely occlude the lumen and lead to downstream ischemia If thepatient survives the initial vascular occlusion, thrombi may becomeorganized and incorporated into the growing plaque.Hemorrhage into a plaque. Rupture of the overlying fibrous cap or ofthe thin-walled vessels in the areas of neovascularization can causeintra-plaque hemorrhage; a contained hematoma may expand theplaque or induce plaque rupture.Atheroembolism. Plaque rupture can discharge debris into thebloodstream, producing microemboli composed of plaque contents.Aneurysm formation. Atherosclerosis-induced pressure or ischemicatrophy of the underlying media, with loss of elastic tissue, causesweakness of the vessel wall and development of aneurysms that mayrupture.
  21. 21. Histologic features of atheromatous plaque in the coronary artery Overall architecture demonstrating fibrous cap (F) and a central necrotic (largely lipid) core (C). The lumen (L) has been moderately narrowed. Note that a segment of the wall is plaque free (arrow), so that there is an eccentric lesion. In this section, collagen has been stained blue (Massons trichrome stain).
  22. 22. Higher power photograph of asection of the plaque shown in A,stained for elastin (black),demonstrating that the internaland external elastic membranes aredestroyed and the media of theartery is thinned under the mostadvanced plaque (arrow).
  23. 23. Acute coronary thrombosis superimposed onan atherosclerotic plaque with focal disruptionof the fibrous cap (arrow), triggering fatalmyocardial infarction
  24. 24. Atherosclerotic plaque rupture. A, Plaquerupture (arrow) without superimposedthrombus, in a patient who died suddenly.
  25. 25. Complicated lesion • The combination of fibrous plaque and the blood clot • occurs when the fibrous plaque breaks open, exposing the cholesterol and connective tissue underneath. This rupture provokes a strong clotting reaction from your blood, such as when you have a cut. is called a complicated lesion.
  26. 26. Atherosclerosis in the aorta. A, Mild Severe disease with diffuse and complicatedatherosclerosis composed of fibrous lesions, some of which have coalesced.plaques (arrow).
  27. 27. Atherosclerosis
  28. 28. Signs and Symptoms Arteries leading to the genitalsArteries leading to leading to the kidneys Arteries the brain Heart arteries
  29. 29. Diagnosis and Tests• Narrowed, enlarged or hardened arteries• Weak or absent pulse• Decreased blood pressure• Whooshing sounds (bruits)• signs of pulsating bulge (aneurysm)• Evidence of poor wound healing
  30. 30. Diagnostic Tests• Blood Tests
  31. 31. • Doppler Ultrasound
  32. 32. • Ankle-Brachial Index
  33. 33. • Electrocardiogram
  34. 34. • Stress Test
  35. 35. • Cardiac catheterization and angiogram
  36. 36. Treatment and Drugs• Eating a healthy diet• Exercise• Quit smoking• Avoid fatty foods• Limit alcohol intake• General check-up
  37. 37. Recommended Medications• Cholesterol medications• Anti-platelet medications• Beta-blocker medications• Angiotensin-converting enzyme (ACE) inhibitors• Calcium channel blockers• Water pills (diuretics)• Other medications
  38. 38. Surgical Procedures• Angioplasty and stent placement
  39. 39. • Endarterectomy
  40. 40. • Thrombolytic Therapy
  41. 41. • Bypass surgery
  42. 42. ATHEROSCLEROSIS Thank you!

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