Flashcards in Thrombus, Embolus, & Atherosclerosis Deck (12):
- the pathologic formation of a blood clot (vs. physiologic)
How can we distinguish a Thrombus from a post-mortem clot?
- via lines of Zahn (alternating lines of RBCs and fibrin)
- via attachment to vessel wall
Give an example of a genetic cause of hypercoagulability.
- mutations in Factor V Leiden prevent its inactivation from Protein S and Protein C, leading to a hypercoagulable state
Protein C and Protein S
- inactivate Factor V and Factor VIII, preventing thrombus formation
- vitamin K dependent; inactivated by warfarin --> there is actually an initial INCREASE in risk of thrombosis as a result, which is why we give heparin at this time
What are the different types of emboli?
- F.A.T. B.A.T.
- fat, amniotic fluid, thrombus, bacteria, air, tumor
What is an atheromatous plaque made up of?
- a necrotic lipid (cholesterol) core with a fibromuscular cap
What happens when an atheromatous plaque ruptures?
- the necrotic contents of the lipid core are exposed, resulting in coagulation --> thrombosis --> partial/total occlusion
Why does atherosclerosis weaken the affected vessel wall?
- because the plaque prevents blood from supplying the deeper parts of the vessel (the media and adventitia), resulting in weakening
What are the three major hypotheses for atheroma formation?
- endothelial injury, oxidative modification of lipids, and a response to retention (lipoproteins retained in the subendothelial space trigger a reaction)
- a macrophage that has phagocytosed a modified (oxidized) lipid/LDL
Pathogenesis of Atherosclerosis
- endothelial injury --> increased blood flow and permeability --> accumulation of lipoproteins and macrophages --> lipids get oxidized --> oxidized lipids get taken up by macrophages --> foam cells and fatty streak --> proliferation of smooth muscle and ECM production --> atherosclerotic genesis