Thrombus, Embolus, & Atherosclerosis Flashcards Preview

Cardiovascular > Thrombus, Embolus, & Atherosclerosis > Flashcards

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)


Foam Cell

- 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


The ECM proliferation during atherosclerosis stabilizes the plaques, so how do these end up potentially rupturing?

- the inflammation causes macrophages to secrete MMPs (matrix metalloproteinases), which breakdown the ECM
- creates unstable plaques that are prone to rupture