Mechanism only, which is the line this course draws against Clinical Medicine and Surgery: how the disease works belongs here, what is done about it belongs there. One idea organizes most of the arterial half. Each artery type is built for a different job, so each fails differently — the elastic aorta loses elastic tissue and DILATES into an aneurysm, the muscular coronary and renal arteries NARROW through atherosclerosis, and the small arteries and arterioles STIFFEN under hypertension. Reasoning from the structure gets you the disease. The neointimal response is the second organizing idea. Injure the endothelium anywhere, by any mechanism, and the same thing happens: smooth muscle migrates into the intima, proliferates, lays down matrix, platelets activate and leukocytes arrive. The wall has a limited repertoire, which is why one process explains in-stent restenosis, transplant vasculopathy and the beginning of every atherosclerotic plaque. Built from the slides. The recording for this lecture is queued behind the exams that come sooner, so every question cites the slide it came from and spoken emphasis will be layered in once the transcript lands.
Answers reveal only after you choose. Your score and a breakdown by objective appear at the end, with a review of everything you missed.