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Hello, everyone. I hope you're all doing well. My name is Rashida and I'm the chairperson at. So welcome to the fifth week of a teaching series. This week we're focusing on vascular surgeon today I surgery. Sorry. Um Today I am joined by Luke who will guide you through major arterial diseases to introduce Luke. He is a final year at the University of Bristol to make the session as engaging as possible. We'll be releasing both throughout these are completely anonymous. So I encourage you to participate actively. If you have any questions during the session, please pop them in the chart and we'll address them at the end of the session. We'll also share a feedback form at the end. If you complete this, you will receive a certificate of attendance and exclusive discount codes to teach me surgery and pass the MRC S. This session is being recorded, the recording and the slides will be shared on a meal page as well as a website, a couple of hours after a session. So please be sure to keep an eye out for that. As you may know, we have launched our very own learning portal which is hosted on our website through this learning portal. You'll get access to practice questions, session recordings and also revision material. As a bonus, all members will get a discount code to 10% of the G kinetics anatomy flashcards, surgical flashcards and knowledge bundle membership is completely free. So be sure to head on to our website after this session to explore this. We also have an exciting opportunity for all of our attendees. Two lucky people will run free access to the GKI metics surgical flashcards at the and the GKI medics a stations to enter, simply complete the Google form at the end of the session and enter the unique code. We will provide the more sessions you attend the higher chances of winning. So be sure to stay until the end of the session and attend as many of our other sessions as well. Finally, before we begin, we'd like to thank our partners, the Royal College of Surgeons England, Kiki Medics, the MDU more than skin deep metal teaching surgery and past the MRC S. Without further ado, I'll now hand it over to Luke. Uh Hi, everyone. Thank you for joining. Uh My name is Luke. I'm a final year medical student from the University of Bristol um I in, in anatomy. Um and I'm actually doing the S FP next year which is vascular them. So this is a good opportunity for me to kind of brush over some of the important uh concepts and conditions. Um So today we're focusing on major arterial disease. Um and I'll kind of just give a brief overview um of what that would involve. Just a quick thank you to the, the partners. Um As said, uh So we'll be covering carotid artery disease, aortic dissection and AAA si won't read out the specific learning objectives, but it will basically be um looking into the patho uh pathophysiology, um investigations and kind of management. Um and looking more into the kind of surgical management and, and how it's approached and things. Uh So in terms of how the session will run, um we'll kind of work top to bottom. So we'll start with carotid artery disease um as a concept. Um We'll then look into endarterectomy, um and the relevant anatomy to that and the anatomy relevant to carotid artery disease itself. Um And then we'll kind of cover the anatomy of the entirety of the aorta. So thoracic and abdominal um before moving on to the clinical uh pathology um of aortic dissection and AAA S, I'm losing my voice a bit as well. So I apologize for that. So we'll make a start. So, um carotid artery disease, um basically refers to this atherosclerotic process um that takes place most commonly in the, the common and the internal carotid arteries. Um It's a, a very similar pathophysiology to car uh coronary artery disease and peripheral arterial disease. Um and therefore, it shares many of the same risk factors. Uh So things such as age, family history, smoking, uh diabetes, obesity, hypertension, things like that. The reason um it's uh you get it at this site um is due to uh slightly more uh turbulent flow at this site due to the bifurcation due to the carotid sinus where you've got a widening of the um the artery. Um So that's why that area is predisposed to um getting atherosclerotic build up. Um And it's actually responsible for about 10 to 15% of ischemic strokes. Um that, that we see um acutely just a, a quick recap of atherosclerosis itself. Um So, usually begins with some degree of um endothelial dysfunction um over kind of your life. Um with various lifestyle risk factors, you get a fatty streak that develops, you get an inflammatory response to that. Um There's migration of some of the smooth muscle um from the tunica media to form this kind of fibrous cap. Um And then that of course, is at risk of rupturing, um which kind of can cause uh the acute events. So, in terms of how carotid artery disease actually presents, the disease itself is usually symptomless. Um in that you're kind of unaware that you're getting this occlusion, you don't get angina as such with co uh coronary artery disease where you get kind of pain associated with narrowing of the lumen. Um Instead, it presents with um an acute um complication, the two main ones obviously are stroke and ti A. Um and obviously on the ti A we've got aurosus few gaps which is this transient, painless vision loss. Um Does anyone know just tug in the chat um clinically how we might distinguish TI A and stroke? I'll give you 10 seconds or so. Um She if you can let me know if anyone comments. Mm, so good duration as in ti A is a short duration. Ok. Yeah, so, so pretty much ti A is classically reversible. Um in that it usually lasts less than 24 hours. I think that's the kind of clinical definition that they run with. Um Meaning that you get some, some kind of stroke like symptom that then resolves within 24 hours. Um A stroke on the other hand, usually leaves you with some kind of permanent paralysis or or disability. Um So those, those are the acute presentations. Um oh actually, before, before I go on to that in terms of how, what, why that happens. Um As I said, when the plaque, uh which obviously narrows the lumen is a risk of rupturing. Um And that reveals this kind of highly thrombogenic surface um to which blood can clot and that's called a thrombus uh where you get occlusion due to blood clotting on a thrombogenic ruptured plaque. Um an embolus on the other hand, um is when part of that blood clot kind of buds off and shoots down and occludes one of the smaller branches um causing uh kind of a more regional stroke. So, if this is the first pole question, if we've got a patient who um has developed over a long period of time and a, a 100% occlusion to one of their carotid arteries, assuming the other one is patent. Um And that there's not been an acute event. How might we expect this to present? So the poll should be up. Um and Reche if you're able to read me out the answers. So, yeah. Mhm So I have, what is the 37% going with a uh Oh, sorry, it's just changed 44% going with a 33% going with B and 18% going with C. Ok. And non, non for d sorry. None, fatigue. No. Ok. Um So it's kind of a um a bit of a leading question in that and sort of a trick question. Um Basically the, the answer is C um And the reason for that is because if you've got an entirely patent contralateral carotid artery, um the the diseased artery can actually occlude and occlude and occlude, not cause any symptoms um to the point where you actually get a full occlusion and can be completely asymptomatic. Um And the reason for that is the circle of Willis. Um So most people will have a patent um kind of patent communicating arteries within the circle of Willis allowing kind of compensatory cross perfusion um with a which actually tho those communicating vessels get stronger as you get an occlusion on one side in response. Um So people can present with eventually a 100% occlusion of one of their carotid arteries and actually be symptomless. Um And in that situation, there's not even much point opening up that artery um because it can actually predispose to some of that clot butting off so that usually leave it. Um It's a slight trick question there. Um But it's, yeah, mo most of you say a I guess if it was causing something, it would be contralateral. Um So yeah, in terms of some other causes of carotid artery disease, um atherosclerosis is kind of the number one cause. Um but we do have a few other differentials. So, carotid dissection. Um classically in an exam question is to be a younger adult. Um It's actually the most common cause of stroke in young adults. Um It classically follows some kind of trauma. So, strangulation um maybe AAA car accident where you've got trauma to the neck. Um and it presents with a unilateral severe neck pain um and kind of headache alongside stroke symptoms. So that's how you would distinguish the two fibromuscular dysplasia. Another differential um obviously a lot rarer than just atherosclerosis. Um But as you can see in the images, um you get this kind of um string of beads appearance, which is like a um