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Buerger disease, also called thromboangiitis obliterans, is a peripheral vascular condition characterized by inflammation of small and medium-sized arteries and veins of the extremities. This inflammation is recurrent, segmental, and non-atherosclerotic, meaning that it’s not caused by atherosclerosis.
All right, let’s go over some physiology. There are three major types of blood vessels: arteries, veins, and capillaries. Normally, blood flows from large arteries into medium and then small arteries called arterioles, which in turn, carry the blood to capillary beds. All arterial vessels have three layers: from outside in, there’s tunica externa or the adventitia layer, which has loose connective tissue; then the tunica media or the media layer, which contains some elastic tissue and smooth muscle that allow the arteriole to dilate or constrict in response to local conditions; and finally, the endothelium, which consists of a single layer of endothelial cells on top of a layer of connective tissue, called lamina propria.
The endothelial cells maintain blood flow by preventing blood cells from reaching the underlying lamina propria. If their continuity is disrupted, blood cells may come up against coagulation factors in the lamina propria. This initiates a coagulation cascade that leads to the formation of a blood clot, which in turn blocks the blood flow.
Now, the arterioles deliver oxygen-rich blood into a network of capillaries, called the capillary bed. Here, oxygen and nutrients pass to tissue cells, which will then return carbon dioxide and wastes back into the capillary bed. These capillaries will then merge to form the smallest veins, called the venules. The structure of these venules is similar to that of arterioles but with thinner walls that contain less smooth muscles. Eventually, these venules drain blood into medium veins, which then drain into large veins that deliver the blood straight back to the heart.
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