X hits on this document

PDF document

Common Congenital Heart Lesions - page 33 / 126





33 / 126

33 of 126

  • This process is mediated by substances secreted by foam cells, activated platelets, and endothelial cells. Examples of this include:

    • o

      PDGF, which is secreted by foam cells and helps to stimulate the migration of SMCs into the subendothelial space.

      • o

        Cytokines (ie. TNF-a, IL-1, TGF-b), which are secreted by foam cells and along with activating WBCs, induces SMC proliferation and ECM protein synthesis.

*Altogether, it is the migration of SMCs from the media to the intima, the

accumulation of WBCs and foam cells, and the formation of the ECM-derived fibrous cap that generates the fibrous plaque characteristic of advanced atherosclerosis.

Fibrous Plaque

  • Localized in the same sites as fatty streaks

  • Appear as firm, gray lesions

  • May project into the lumen, and if large enough, create a significant stenosis or obstruction to blood flow

  • Has a necrotic core of cellular debris, as a result of the toxic effects of mLDL and of free oxygen radicals & hydrolytic enzymes derived from foam cells and T cells

  • Thrombogenic due to its necrotic core. This is attributed to:

    • o

      Production of TF by foam cellsÆ activation of coagulation

      • o

        Release of PDGF by activated plateletsÆ degradation of heparin sulfate, a compound normally involved in the inhibition of SMC migration and proliferation.

3. Differentiate the clinical presentation and pathophysiology of coronary artery stenosis from coronary artery thrombosis

...So, I couldn’t find any specifics in the book about this nor was there anything specific in the powerpoint lectures…I’ll email Dr. Smith for key points and get back to you…

Document info
Document views489
Page views489
Page last viewedTue Jan 24 08:09:51 UTC 2017