the pathology presentation in UoB (2).pptx

the pathology presentation in UoB (2).pptx

• 2.
  Presentation of pathology Grouptwo
• 3.
   Vascular wallis the layered structure of blood vessels,mainly arteries and veins.  It is built and maintained by coordinated activity of endothelial cells smooth muscles cells and fibroblast supported by extracullar matrix production.  It maintains structural integrity and elasticity of the blood vessels and regulates blood flow and hemostatis and support vascular repair after injury. Vascular wall synthesis
• 4.
   Blood vesselsespecially arteries have three main layers.  Tunica intima :inner most layer in contact with blood and provides smooth surface to reduce clotting.  Tunica media: middle muscular layer made mainly of smooth muscle cels and elastic fibers and provides elasticity and strength.  Tunica adventitia:outer connective tissue layer containing collagen fibers ,fibroblast and vasa vasorum and provides structural support. Basic structure of the vascular wall
• 5.
   Endothelial cells:arespecialized flattened cells that line endothelium and maintaining vessel wall homeostasis and circulatory function  It contain weibel-palade bodies :storage organelles for von willebrand factor(vWF) important for platelet adhesion in clotting.  Main function :provide non thrombogenic surface and prevents blood clotting under normal condition.  It release anticoagulant molecules such as prostacyclin,nitric oxide and thrombomodulin  It control vascular tone and regulate permeability. The two main cell types
• 6.
   Vascular smoothmuscles cells:found mainly in tunica media and arranged in concentric layer around the lumen.  Main function:regulate blood vessel diameter( vasocontriction and vasodilation)  It participate in both normal vascular repair and pathological processes such as atherosclerosis.  It release growth factor and cytokines and repair vessel wall after injury.  It produce ECM(collagen,elastin and proteoglycan. Vascular smooth muscle cells
• 7.
   Vascular injuryleading to Endothelial loss or dysfunction stimulates Smooth muscle cell growth, Extracellular matrix synthesis, and thickening of the vascular wall.  Healing of injured vessels involves the migration of SMCs or SMC precursor cells into the intima. These cells then proliferate and synthesize ECM. VASCULAR WALL RESPONSE TO INJURY
• 8.
  forming a neointimathat typically is covered by an intact EC layer. This neointimal response occurs with any form of vascular damage or dysfunction, including infection, inflammation, immune injury, physi cal trauma (e.g., from a balloon catheter or hypertension), or toxic exposure (e.g. oxidized lipids or cigarette smoke). Thus, intimal thickening is a stereotypical response of the vessel wall to any insult. cont
• 9.
  the phenotype ofneointimal SMCs is distinct from medial SMCs. Thus, neointimal SMCs are not contractile like medial SMCs, but do have the capacity to divide and have a considerably greater synthetic capacity than their sleepy colleagues in the media. The migratory, proliferative, and synthetic activities of the intimal SMCs are regulated by growth factors and cytokines produced by platelets, ECs, and macrophages, as well as by activated coagulation and complement factors cont
• 10.
  With restoration and/ornormalization of the EC layer, intimal SMCs can return to a nonproliferative state, but not before the healing response has produced intimal thickening. With persistent or recurrent insults, further thickening can occur that leads to the stenosis of small- and medium sized blood vessels. cont