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My book( textbook of anatomy abdomen and lower limb 2nd edition - by vishram Singh pg.no:286) says:

Acute arterial occlusion: It is mostly caused by embolism or thrombosis. It usually occurs in the femoral artery where it gives off the profunda femoris artery.

So my question what makes this site more susceptible for atherosclerosis? In general what are factors that make some sites more susceptible to atherosclerosis?

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  • $\begingroup$ Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning. There is plenty of information on atherosclerosis available easily online, starting with Wikipedia. $\endgroup$
    – MattDMo
    Dec 18, 2016 at 16:19

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I can give you some facts about atherosclerosis, but I should warn you that--judging by your question--you may be making a false equivalence between atherosclerosis thrombus/embolism. The two are often very interrelated, but there are times when an atherosclerotic plaque is significant without causing an embolism (e.g. stable angina) and there are times when a thromboembolism forms without the presence of a significant atherosclerotic plaque (e.g. atrial fibrillation). The likelihood of thrombus formation is dictated by Virchow's Triad: Endothelial Dysfunction, Blood stasis/turbulence, inherent coagulability of the blood (factor problems mostly).

Now to get to your main question: atherosclerosis. The current theory is called The Response to Injury Theory. The general idea is that whenever there is damage to endothelial cells they will release inflammatory cytokines, and these will lead to a thickening of the wall. There are a lot of different things that can lead to this endothelial damage. There chemical factors: exogenous sources like cigarette smoke and endogenous sources like elevated levels of homocysteine. However the two most important factors that lead to endothelial damage are high cholesterol and hemodynamic factors (Robbins, 494). That second point hints at why atherosclerotic plaques are more common at branch points. As blood is going past a branch point it becomes more turbulent which makes it more likely to cause damage. This is especially true when blood is flowing more forcefully, as in the case of hypertension (another risk factor for the development of atherosclerotic plaques).

There are many other factors that play into the development of atherosclerotic plaques. For example, the abdominal aorta distal to the renal arteries has no vasa vasorum, which makes it more susceptible plaque formation(5). This is just a small sample though. There are a plethora of factors that go into plaque formation: literally textbooks full of information about he disease. If you're really interested in the topic and want to dive in, I'd suggest taking a look at Inflammatory Atherosclerosis.

Progression of Atherosclerotic Plaques - Robbins and Cotran Pathologic Basis of Disease 9th Ed. - 495

Evolution of arterial wall changes in the response to injury hypothesis. 1, Normal. 2, Endothelial injury with monocyte and platelet adhesion. 3, Monocyte and smooth muscle cell migration into the intima, with macrophage activation. 4, Macrophage and smooth muscle cell uptake of modified lipids, with further activation and recruitment of T cells. 5, Intimal smooth muscle cell proliferation with extracellular matrix production, forming a well-developed plaque. (Kumar 495)

Kumar, Vinay, Abul Abbas, Jon Aster. Robbins & Cotran Pathologic Basis of Disease, 9th Edition. Saunders, 062414. VitalBook file.

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