CVD

• atherosclerosis- hardening of arteries

  1. damage eg high blood pressure to the endothelium wall of an artery
  2. inflammatory response occurs and WBCs accumulate in damaged area
  3. lipids cholestrol and WBC clump together under endothelium causing an atheroma
  4. platelets add to fatty deposits- forming plaque
• effects of atherosclerosis

  • atheroma/plaque narrows th lumen, restricting blood flow and increasing BP
  • plaque can harden and reduce elasticity of artery further increasing BP

  positive feedback
• thrombosis


  prevents excess blood loss, entry of pathogens, allows healing

  1. damage to blood vessels exposes collagen fibres, platelets attracted to fibres and release thromboplastin(protein)
  2. thromboplastin triggers conversion of inactive prothrombin(protein) into active thrombin(enzyme)
  3. for this conversion, calcium ions and vitamin K must be present(clotting factors)
  4. thrombin catalyses conversion of soluble fibrinogen into insoluble fibrin
  5. fibrin forms a network/mesh net of fibres, trapping RBCs and platelets= blood clot
• blood clots and atheromas

  • plaque deposits can rupture through endothelium triggering thrombosis
  • blood clot could completely block artery
  • blood clot can dislodge and travel to different areas of body including brain(stroke) and heart (heart attack)
• stroke

  • sudden loss of brain functiion due to decreased blood flow, less 02 less aerobic respiration and decrease ATP production/energy
  • reducing brain cell function
• heart attack


  coronary heart disease= formation of atheromas or blood clots in coronary artery

  1. decreased blood flow
  2. decreased 02 to cells
  3. decreased aerobic respiration
  4. no longer producing ATP so decreased contractions- less force fro m heart
  5. cells can die leading to permanent damage to heart tissue or cause a heart attack